bio europe fall 2026: EADV 2026 Biotech BD Preview

EADV 2026 Preview: Immunotherapy for Skin Diseases Moves Toward More Precise Disease Control

 —Pre-Congress Insights on the 35th European Academy of Dermatology and Venereology Congress (EADV Congress 2026)

 The 35th Congress of the European Academy of Dermatology and Venereology (EADV Congress 2026) is scheduled to take place in Vienna, Austria, from September 30 to October 3, 2026. Biologics and small molecules such as JAK inhibitors have expanded treatment options for autoimmune skin diseases; the next phase of competition will hinge on the ability to enhance tissue and cellular selectivity, reduce systemic immunosuppression, prolong remission, and lower the long-term burden of treatment.The rise of bispecific antibody-drug conjugates (ADCs) and non-oncology ADCs signals that precision delivery is expanding beyond oncology, raising the question of whether dermatological immunotherapy might shift from pathway inhibition toward cell-targeted interventions. This article presents a pre-congress preview organized into nine sections, covering four perspectives: clinical, translational, R&D, and business development. The business development forum that anchors autumn biopharma dealmaking—most visibly bio europe fall 2026—frames the licensing and partnership agenda that EADV’s clinical readouts later stress-test.

 1. The focus of EADV 2026 has shifted from the mere presence of new drugs to whether treatments are sufficiently precise—and why that question matters beyond bio europe fall 2026

 The 35th European Academy of Dermatology and Venereology (EADV) Congress 2026 is scheduled to take place from September 30 to October 3, 2026, in Vienna, Austria. The EADV is one of the largest academic conferences in the field of dermatology and venereology in Europe, covering clinical practice, basic research, translational medicine, and continuing education. It attracts dermatologists, researchers, and industry representatives from across Europe and beyond each year.The official conference website (https://eadv.org/) has officially announced the dates and host city for the 2026 event.

 The focus of this year’s EADV has shifted from “whether new drugs will be launched” to “whether treatments are sufficiently precise.” Over the past decade, treatment options for autoimmune skin diseases have expanded significantly due to the successive launch of biologics and small-molecule therapies such as JAK inhibitors:Monoclonal antibodies targeting IL-17, IL-23, IL-4/13, and TSLP have been successively introduced for indications such as psoriasis, atopic dermatitis, hidradenitis suppurativa, and prurigo nodularis; JAK inhibitors such as tofacitinib, baricitinib, upatitinib, and abuxitinib cover a wide range of skin diseases. However, an increase in treatment options does not automatically translate to improved treatment quality.The questions dermatologists will need to address at the 2026 EADV conference will focus more on: Is the cost of long-term immunosuppression justified? Which patients can achieve deep remission, and which are prone to relapse? Do new targets and molecular structures offer clinical benefits, or are they merely a rebranding?

 When using the registration figures for the 2025 EADV (publicly reported at over 12,000 attendees, held in Paris) as a reference, it is important to note that this number is based on actual attendance statistics from 2025; the final attendance figures for 2026 will be subject to the data released by the EADV officially before and after the conference. This article does not use attendance size as an indicator of the conference’s value but rather takes the conference program and agenda as the starting point for analysis.The following sections are organized into nine chapters, covering the costs of long-term management, patient stratification, JAK selectivity, non-oncology ADCs, China’s bispecific ADC transactions, attendee perspectives, the boundaries of evidence, conclusions, and frequently asked questions.

 1.1 Both Biologics and Small Molecules Must Address the Cost of Long-Term Management

 Drugs for treating autoimmune skin diseases can currently be divided into two major categories: large-molecule biologics (primarily monoclonal antibodies) and small-molecule oral medications (represented by JAK inhibitors). Each category has its own advantages and trade-offs; long-term control requires a simultaneous assessment of “whether the trade-offs are acceptable” across multiple dimensions, and comparing the speed of onset alone is insufficient for evaluation.

 Representative biologics include: IL-17 inhibitors (secukinumab, ixekizumab, brolizumab), IL-23 inhibitors (guselkumab, risekizumab, teclizumab),IL-12/23 inhibitors (usnulumab), IL-4/13 inhibitors (duplixent), and TSLP inhibitors (tezolizumab), among others.Representative JAK inhibitors include: tofacitinib (JAK1/3), baricitinib (JAK1/2), upatitinib (JAK1), abuxitinib (JAK1), degositinib (JAK1), and the selective TYK2 inhibitor deuterated baricitinib, among others.Each drug differs in terms of onset of action, duration of remission, relapse rate after discontinuation, risk of infection, laboratory monitoring requirements, treatment burden, and management considerations for specific patient populations; therefore, they cannot be simply generalized under the umbrella terms “biologics” or “JAK inhibitors.”

 Table 1-1 Comparison of Onset of Action and Duration of Response Between Biologics and JAK Small Molecules (Compiled from Published Clinical Trial Data)

Dimension	IL-17 Inhibitors	IL-23 Inhibitors	IL-12/23 Inhibitors	JAK Inhibitors
Time to Onset of Action	Noticeable improvement seen within 2–4 weeks	Peak effect reached in 8–12 weeks	Peak effect reached in 12–16 weeks	Improvement in itching is visible within 1–2 weeks
PASI 90 (16 weeks)	Approximately 60%–70%	Approx. 70%–80%	Approx. 50%–60%	Psoriasis-related symptoms: approximately 40%–50%
Median time to relapse after discontinuation	12–16 weeks	24–48 weeks	20–30 weeks	4–8 weeks
Route of administration	Subcutaneous injection	Subcutaneous injection	Subcutaneous injection	Oral
Frequency During Maintenance Phase	Once a month	Every 8–12 weeks	Once every 12 weeks	Once or twice daily

 In terms of onset of action, improvements in itching and skin lesions are typically observed within 1–2 weeks after administration of JAK inhibitors; in patients with atopic dermatitis, a reduction in itching scores can be seen as early as the first week with upatilinib;Biologics take slightly longer to take effect; IL-17 inhibitors typically show marked improvement in psoriasis patients within 2–4 weeks, while IL-23 inhibitors take longer to take effect but provide longer-lasting remission. A rapid onset of action is associated with higher patient adherence, but a rapid onset does not necessarily equate to long-term control.Ustekinumab can maintain remission for up to 5 years, and the VOYAGE trial of guselkumab showed a 5-year treatment retention rate exceeding 80%; in contrast, relapse following discontinuation of JAK inhibitors typically occurs within 4–8 weeks after stopping treatment. Re-initiation of treatment after relapse may still be effective, but the depth of remission may diminish.

 Table 1-2: Cost-Benefit Analysis of Long-Term Control (Comparison by Dimension)

Cost Dimension	Biologics	JAK Inhibitors
Risk of Infection	Generally low; IL-17 inhibitors are associated with a slightly increased risk of candidiasis	Increased risk of herpes zoster (utofatinib); opportunistic infections require monitoring
Tuberculosis reactivation	Higher risk with TNF inhibitors; lower risk with newer biologics	All JAK inhibitors require baseline screening and monitoring
Cardiovascular events	TNF inhibitors may increase the risk of heart failure; no significant increase has been observed with newer biologics	Increased MACE in the Tofacitinib ORAL Surveillance trial
Malignant tumors	Long-term data have not shown a significant increase	An increase was observed with tofacitinib in patients aged 50 and older with cardiovascular risk factors
Laboratory Monitoring	Baseline screening for tuberculosis, hepatitis B, and hepatitis C; regular follow-up	Routine monitoring of complete blood count, liver and kidney function, and lipid profile is required
Administration Burden	Subcutaneous injection, once monthly to once every 12 weeks	Oral administration once or twice daily, but frequent monitoring is required
Immunogenicity	Some drugs may induce drug-neutralizing antibodies	No issues with neutralizing antibodies, but rapid relapse upon discontinuation

 The burden of administration is another often underestimated factor. Among biologics, secukinumab requires a monthly subcutaneous injection during the maintenance phase, gusecimumab is administered every 8 weeks, and usulimumab every 12 weeks; JAK inhibitors are taken orally once or twice daily, requiring no injections but necessitating long-term monitoring. Patient preferences vary significantly: younger, more active patients prefer oral formulations;whereas older patients, those with multiple chronic conditions, or those already taking numerous medications may actually be more receptive to injectable formulations. Management considerations differ for special populations: pregnant women are generally advised to avoid JAK inhibitors and most biologics; JAK inhibitors should be used with caution in older patients with cardiovascular risk factors, particularly tofacitinib; and patients with active tuberculosis or chronic hepatitis B must receive prophylactic treatment before starting TNF inhibitors or JAK inhibitors.

 Table 1-3 Key Management Points for Special Populations (Comparison of Biologics and JAK Inhibitors)

Special Populations	Key Management Points for Biologics	Key Management Points for JAK Inhibitors
Pregnant Women	Pexelizumab has a favorable safety profile; discontinuation of other biologics is recommended during the second and third trimesters	Not recommended; discontinue treatment at least 4 weeks before conception
Breastfeeding Women	Most biologics are excreted into breast milk; individual assessment is required	Not recommended
Elderly patients (≥65 years)	Overall safety is good; monitor for infections	Use tofacitinib with caution; JAK1-selective inhibitors or biologics may be considered
Concomitant cardiovascular risk	Avoid TNF inhibitors in patients with heart failure	Avoid tofacitinib; monitor for VTE risk with upatitinib and similar agents
Latent tuberculosis	Prophylactic antituberculosis therapy is required prior to initiating TNF inhibitors; screening is still recommended for newer biologics	Prophylactic anti-tuberculosis therapy is required prior to all JAK inhibitors
Hepatitis B virus carriers	Prophylactic antiviral therapy is required before initiating TNF inhibitors; new biologics require individual assessment	Prophylactic antiviral therapy (entecavir or tenofovir) is required
Pediatric patients	Some biologics have been approved for pediatric use	Some JAK inhibitors have been approved for pediatric atopic dermatitis

Recommendations for Action: In on-site reports at EADV 2026, clinicians should document data on time to response, depth of remission, relapse rates after discontinuation, infection events, monitoring frequency, treatment burden, and safety in special populations, and avoid being misled by labels such as “new target” or “new molecule.”Whether a new drug is worth incorporating into clinical practice depends on whether it offers a better balance between long-term control and treatment costs in the patient population you treat.

 1.2 Visible Skin Changes Do Not Equate to Simple Efficacy Assessment

 At first glance, evaluating the efficacy of treatments for skin diseases seems straightforward: skin lesions are visible on the skin, can be observed with the naked eye, documented through photographs, and scored. However, in clinical practice, relying solely on lesion scoring to judge efficacy equates “the skin looks better” with “the patient is truly better”—an equivalence that is unreliable in the long-term management of autoimmune skin diseases.

 Skin lesion scoring tools include: PASI (Psoriasis Area and Severity Index),EASI (Eczema Area and Severity Index), IGA (Investigator’s Global Assessment), BSA (Body Surface Area), SCORAD (SCORing Atopic Dermatitis), and HI-Score (Hidradenitis Suppurativa Score), among others.These scoring systems are used as primary endpoints in clinical trials, but each has its limitations: PASI is not sensitive to lesions in specific areas such as the scalp, nails, and genitalia; EASI primarily reflects erythema, papules, scratch marks, and lichenification, and does not directly assess itching; IGA is a static, overall assessment that struggles to reflect a fluctuating disease course; and BSA does not assess the patient’s subjective experience at all.

 Table 1-4 Comparison of Commonly Used Skin Lesion Scoring Tools

Scoring Tool	Applicable Diseases	Main Dimensions	Limitations
PASI	Psoriasis	Erythema, infiltration, scaling, area of involvement	Not sensitive to scalp, nails, or genital involvement; does not assess itching or PRO
EASI	Atopic dermatitis	Erythema, papules/scratch marks, lichenification, area of involvement	Itching is not directly assessed; calculation methods differ for children and adults
IGA/vIGA	Various skin conditions	Overall severity (0–4 or 0–5)	Static assessment; does not reflect a fluctuating course of the disease
BSA	Various skin diseases	Percentage of body surface area affected	Does not assess severity; does not assess PRO
SCORAD	Atopic dermatitis	Objective skin lesions + subjective symptoms	The subjective component relies on the patient’s recollection
HI-Score	Pyoderma of the sweat glands	Nodules, abscesses, drainage tracts	Insufficient assessment of pain and quality of life

 The true burden of disease for patients with autoimmune skin diseases far exceeds what skin lesion scores can capture.Itching in patients with atopic dermatitis typically worsens at night, affecting the ability to fall asleep and stay asleep; chronic sleep deprivation leads to decreased attention, emotional problems, and reduced work productivity. In addition to itching, patients with psoriasis may experience joint pain, impaired fine motor skills due to nail damage, as well as feelings of shame, social withdrawal, and depression and anxiety caused by visible skin lesions;Pain in patients with hidradenitis suppurativa is often underestimated; nodules, abscesses, fistulas, and scarring lead to limited mobility and a significant increase in work absenteeism. Patient-Reported Outcomes (PROs) were established precisely to address the blind spots in skin lesion scoring.

 Table 1-5 Dimensions of Commonly Used Patient-Reported Outcomes (PRO) Scales

PRO Scale	Assessment Dimensions	Applicable Conditions	MCID Reference
NRS Itch	Itch Severity (0–10)	Atopic dermatitis, nodular prurigo	Improvement of ≥4 points
POEM	Patient-Reported Eczema Severity (Past Week)	Atopic dermatitis	Improvement of ≥3.4 points
DLQI	Dermatology Quality of Life Index (10 items)	Various Skin Conditions	Improvement of ≥4 points
EQ-5D	European Quality of Life Questionnaire-5 Dimensions	General Health-Related Quality of Life	Improvement in utility values
WPAI	Work Productivity and Activity Impairment	Multiple Chronic Skin Conditions	Percentage Improvement
PQoL	Psoriasis Quality of Life Questionnaire	Psoriasis	Improvement Score
HiSQoL	Quality of Life in Pyoderma	Pyoderma of the sweat glands	Improvement in Scores

 Commonly used PRO scales include: NRS (Numerical Rating Scale) for itching (0–10), PSA (Sleep Scale), DLQI (Dermatology Life Quality Index), EQ-5D (European Quality of Life Questionnaire), WPAI (Work Productivity and Activity Impairment Questionnaire), POEM (Patient-Obedience Eczema Measure), PQoL (Psoriasis Quality of Life Questionnaire),HiSQoL (Quality of Life in Pyoderma), among others. Clinical studies for EADV 2026 should report both lesion scores and PROs; otherwise, they only address “how the skin looks” rather than “how the patient feels.”

 Short-term improvement in skin lesions does not equate to long-term benefit. Clinical trials often set 12–16 weeks as the primary endpoint, but autoimmune skin diseases have a chronic course. Whether relapse occurs after discontinuation, how long remission lasts, and whether retreatment remains effective are more important than short-term lesion clearance rates.The VOYAGE 2 trial of guselkumab showed a median remission duration of approximately 28 weeks after discontinuation; the IMMhance trial of usulimumab demonstrated that some patients maintained remission for over a year after discontinuation;relapse typically occurs within 4–12 weeks after discontinuation of IL-17 inhibitors; relapse occurs more rapidly after discontinuation of JAK inhibitors. These differences in “post-discontinuation outcomes” are not evident in short-term trials and must be assessed through extension studies and real-world data.

 Table 1-6: The Gap Between Short-Term Lesional Improvement and Long-Term Benefits

Dimension	Short-Term Trials (12–16 Weeks)	Long-Term Follow-Up (≥1 Year)	Source of Discrepancy
Remission Rates	Peak PASI 90/EASI 75	Decrease in maintenance rate	Relapse in some patients after discontinuation
Improvement in PROs	Rapid improvement in itching and quality of life	Rebound may occur	PRO improvements are not synchronized with improvements in skin lesions
Safety	Initially high rate of adverse events	Cumulative rate of long-term events	Rare adverse events require long-term exposure
Post-discontinuation Findings	Typically not evaluated	Median time to recurrence can be measured	Requires a specific treatment discontinuation and follow-up design
Response to retreatment	Not typically assessed	Possible response decline	Repeated treatment discontinuation and retreatment may result in ADA

Recommendations for Action: When reviewing abstracts from EADV 2026, clinicians should simultaneously verify the type of primary endpoint (lesion score vs. PRO), the duration of follow-up (whether ≥1 year), whether remission maintenance after discontinuation is reported, whether the efficacy of retreatment is reported, and whether data on specific patient subgroups are included. Focusing solely on PASI 90 or EASI 75 at 12 or 16 weeks may overestimate the drug’s true value in long-term management.

 2. Once biologics enter a phase of mature competition, patient stratification becomes more important than adding new targets

 Biologic therapy for autoimmune skin diseases has entered a phase of “mature competition.” Targets such as IL-17, IL-23, IL-12/23, IL-4/13, and TSLP already have approved drugs on the market, and the differences in efficacy between drugs within the same class are narrowing.In this context, the marginal value of simply adding new targets is declining. More important than adding targets is determining “which patients are best suited for which drug”—that is, patient stratification. This chapter explores two perspectives—post-discontinuation outcomes and multi-target design—to illustrate how, in the mature competition phase, the logic of stratification surpasses the number of targets to become the core of a new drug’s value.

 2.1 High Remission Rates Must Be Interpreted in Conjunction with Post-Discontinuation Performance

 Response rates in clinical trials (such as PASI 90, PASI 100, EASI 75, and EASI 90) reflect the peak efficacy of a drug in the short term, but they do not tell the whole story. It is one thing for a drug to achieve PASI 90 in 70% of patients at 12 or 16 weeks; it is an entirely different matter for that same drug to help patients maintain remission 2 or 5 years later.When reviewing EADV 2026 abstracts, clinical teams should also note the duration of follow-up, the proportion of sustained responses, studies on dosing intervals and dose optimization, the median time to relapse after discontinuation, the response rate upon re-treatment, and the incidence of anti-drug antibodies.

 IL-23 inhibitors demonstrate excellent post-discontinuation maintenance in psoriasis: The VOYAGE 1 and VOYAGE 2 extension studies of guselkumab showed that the median duration of remission after discontinuation was approximately 28 weeks, with some patients maintaining remission for more than 48 weeks;The IMMhance trial of risatuzumab showed a median duration of PASI 90 maintenance after discontinuation of approximately 35 weeks; the IMMpress trial of teclizumab showed that approximately half of patients remained in remission 6 months after discontinuation.In contrast, IL-17 inhibitors show shorter duration of remission after discontinuation: the median time to relapse after discontinuation of icizumab is approximately 16 weeks; for secukinumab, relapse occurs approximately 12 weeks after discontinuation. Ustekinumab falls between the two, with a median duration of remission of approximately 20–30 weeks after discontinuation.

 Table 2-1 Comparison of Post-Discontinuation Performance of Major Biologics

Drug Class	Representative Drugs	Median Time to Relapse After Discontinuation	Response to Retreatment	Antibody Resistance Rate
IL-23 Inhibitors	Gusecliumab	Approx. 28 weeks (some 48 weeks+)	Most patients can still achieve the depth of their initial remission	<5%
IL-23 inhibitors	Rizumab	Approximately 35 weeks	Still effective	<5%
IL-23 inhibitor	Tecotromab	Approx. 24 weeks (half of patients maintained response for 6 months)	Still effective	<5%
IL-12/23 Inhibitors	Usunumab	Approx. 20–30 weeks	Still effective	<5%
IL-17 inhibitors	Secukinumab	Approximately 12 weeks	Still effective, with a slight decline in a small number of cases	Approx. 5%–8%
IL-17 Inhibitors	Eculizumab	Approximately 16 weeks	Still effective	Approximately 5%–10%
IL-4/13 inhibitors	Dupilumab	Approx. 8–12 weeks	Still effective	<3%

 There is a trade-off between extending the dosing interval and the risk of relapse. The standard maintenance regimen for guseliumab is every 8 weeks; some studies have attempted to extend this to every 12 weeks, finding that some patients can still maintain remission, but the overall relapse rate increases. The standard regimen for usnumab is every 12 weeks, and for some patients, this can be extended to every 16 weeks. The standard regimen for secukinumab is once monthly, and relapse occurs relatively quickly after discontinuation.The efficacy of retreatment also warrants attention: when the same drug is re-administered after discontinuation, most patients can still achieve a depth of remission similar to that of the initial treatment; however, some patients who repeatedly discontinue and then resume treatment may develop anti-drug antibodies (ADAs), leading to a decline in response and necessitating a switch to other therapeutic targets.

 Table 2-2: Risk of Relapse Associated with Extended Dosing Intervals (Summarized by Drug)

Drug	Standard Maintenance Period	Studies on Extended Dosage Intervals	Risk of Relapse After Extension	Eligible Patients
Gusecimab	Every 8 weeks	Every 12 weeks	Maintenance therapy may be used in some patients; overall relapse rate increases	Patients with a stable remission of ≥1 year
Usunumab	Every 12 weeks	Every 16 weeks	Some patients may continue maintenance therapy	Patients with a stable remission for ≥1 year
Rizumab	Every 8 weeks	Every 12 weeks	Limited data	Requires individual assessment
Secuquimab	Once a month	Observation after discontinuation	Relapse within 12 weeks of discontinuation	Routine discontinuation is not recommended
Ixizumab	Once every 4 weeks	Once every 8 weeks	Remission may wane in some patients	Requires individual assessment
Dupilumab	Every 2 weeks	Withdrawal and observation	Relapse 8–12 weeks after discontinuation	Routine discontinuation is not recommended

 The greater the need for long-term treatment, the more important it is to consider convenience, immunogenicity, and accessibility when comparing products. For patients requiring long-term, continuous treatment, an injection every 8 weeks is more convenient than one every month; patients seeking the convenience of oral medication prefer JAK inhibitors; economic accessibility varies significantly across countries—biologics are more accessible in Europe and Japan, where health insurance coverage is robust, whereas accessibility is limited in markets with higher out-of-pocket costs.The incidence of anti-drug antibodies (ADAs) is often overlooked in long-term management: a high incidence of ADAs may lead to diminished efficacy, injection-related reactions, and accelerated relapse after discontinuation, and is a critical quality indicator for the long-term use of biologics.

 Table 2-3 Checklist for Assessing Long-Term Treatment Needs

Assessment Dimensions	Question	Data Source
Duration of Follow-up	Is the trial follow-up period ≥ 1 year? Is it ≥ 3 years?	ClinicalTrials.gov Registration
Sustained Response	Week 52 PASI 90/EASI 90 maintenance rate?	Primary/Secondary Endpoints
Dose optimization	Are there studies on extended dosing intervals?	Trial Design and Extension Studies
Relapse After Discontinuation of Treatment	What is the median time to relapse after discontinuation?	Discontinuation-Follow-up Substudy
Response to Retreatment	Is retreatment effective after discontinuation?	Retreatment Substudy
Drug-Resistance Antibodies	What is the incidence of ADA? Does it affect efficacy?	Immunogenicity Substudy
Accessibility	Health insurance coverage? Out-of-pocket costs?	National Health Insurance Reimbursement Lists

 Recommendations: When reviewing response rate data from EADV 2026, clinical teams should also document the duration of follow-up, the proportion of sustained responses, studies on dosing intervals and dose optimization, the median time to relapse after treatment discontinuation, the response rate upon retreatment, and the incidence of anti-drug antibodies. Focusing solely on response rates without considering post-treatment outcomes may overestimate the drug’s value in real-world long-term management.

 2.2 Multi-target Designs Must Demonstrate Clinical Benefit

 The design philosophy of biologics has evolved from early single-target monoclonal antibodies (such as the TNF inhibitors infliximab, adalimumab, and etanercept) to today’s bispecific antibodies, multifunctional molecules, and antibody-drug conjugates. While structures are becoming increasingly complex, “greater structural complexity” does not equate to “a more advanced mechanism of action,” much less “better clinical outcomes.”Multi-target designs must be validated by clinical data to demonstrate that they indeed provide clinical benefits that cannot be achieved with single-target approaches.

 The clinical benefits of a dual-target design may arise from three pathways: First, simultaneously blocking two disease-causing pathways to cover a broader patient population (e.g., a TNF/IL-17 bispecific antibody could theoretically control both the inflammatory and neutrophil pathways at the same time); second, enhancing tissue selectivity through synergistic endocytosis of the dual targets (a common rationale for bispecific antibody-drug conjugates, or ADCs);third, by simultaneously blocking soluble ligands and membrane receptors to reduce escape mechanisms (e.g., the IL-13/TSLP bispecific antibody). All three approaches require validation: Are both targets clinically meaningful in the same patient and at the same disease stage? Does the exposure to both targets support synergy? Do the additional toxicities offset the benefits?

 Table 2-4 Comparison of Single-Target and Dual-Target Designs

Dimension	Single-Target Monoclonal Antibodies	Bispecific Antibodies	Validation Requirements
Design Logic	Blocking a Single Signaling Pathway	Simultaneous Blockade of Two Signaling Pathways	Must demonstrate that both pathways are clinically relevant in the same patient
Manufacturing Complexity	Relatively simple	High (heavy-chain/light-chain mismatch)	Requires process optimization and consistency validation
Endocytosis efficiency	Depends on target characteristics	May be synergistically enhanced	Requires in vitro and in vivo validation
Selectivity	Depends on target expression	May increase or decrease	Tissue distribution data required
Toxicity profile	Relatively clear	May be broader	Adverse event monitoring is required
Clinical endpoints	Established standards	Must demonstrate superiority over single-target therapy	Head-to-head or superiority design required

 Criteria for determining clinical benefit include: faster onset of action, deeper remission, longer remission duration, lower relapse rate after discontinuation, comparable or superior safety, comparable or lighter treatment burden, and greater safety in specific patient populations.A treatment can be considered to have “clinical benefit” only if it demonstrates significant superiority over the current standard of care in at least one of these metrics, without significant deterioration in any other metrics. The “dual-target” label alone does not constitute clinical benefit, nor does a “new mechanism” alone.

 Table 2-5: Dimensions for Assessing Clinical Benefit

Dimension	Assessment Criteria	Data Requirements
Onset of Action	Significantly faster than the control (e.g., within 4 weeks vs. within 8 weeks)	Primary Endpoint Time Point
Depth of Remission	Significantly higher proportion achieving PASI 100/EASI 100	Primary Endpoint
Response Duration	Significantly higher 52-week maintenance rate	Extension phase data
Maintenance after discontinuation	Significantly prolonged median time to relapse	Discontinuation-to-Follow-Up Substudy
Safety	Rate of serious adverse events was comparable or lower	Safety database
Administration Burden	Frequency comparable or lower	Dosage regimen
PRO Improvement	Improvement in itch NRS and DLQI Equivalent or better	Secondary Endpoints
Special populations	Data for elderly, pediatric, and patients with comorbidities were comparable or better	Subgroup Analysis

 Cases where toxicity outweighs benefits are not uncommon. Dual-target therapies that simultaneously block two immune pathways may result in broader immunosuppression and an increased risk of infection; ADCs that simultaneously target two tumor-associated antigens may lead to increased off-target toxicity because normal tissues also express one of the targets;Bispecific antibodies that simultaneously block IL-4/13 and TSLP could, in theory, cover both major pathways involved in atopic dermatitis, but may increase the risk of parasitic or opportunistic infections due to excessive suppression of Type 2 immunity. These risks must be verified in clinical data rather than inferred solely from mechanisms of action.

 Table 2-6 Examples of Toxicity Offsetting Benefits (Mechanistic Inference and Clinical Observations)

Design	Mechanism-Based Benefits	Mechanism-Based Risks	Clinical Validation Requirements
TNF/IL-17 Bispecific Antibody	Simultaneous Control of Inflammation and Neutrophils	Cumulative Risk of Infection	Monitoring of Infection Incidence
IL-13/TSLP Bispecific Antibody	Covers dual pathways of Type 2 immunity	Excessive suppression of Type 2 Immunity	Monitoring for Parasitic/Opportunistic Infections
IL-17/IL-23 bispecific antibody	Covers upstream and downstream pathways	Combination of immunosuppressive therapies	Infection monitoring
Dual-Target ADCs	Enhanced selectivity for tumor/pathogenic cells	Toxicity caused by expression in normal tissues	Tissue Distribution and PK/PD
PD-1/CTLA-4 Bispecific Antibodies	Enhancing Antitumor Immunity	Increased immunotoxicity	irAE Monitoring

 Action Recommendations: In presentations on bispecific or multifunctional molecules at EADV 2026, both clinical and R&D teams should ask: Is there causal evidence for both targets in human disease? Does simultaneous inhibition of both targets lead to improvements in clinical endpoints? Does the spectrum of adverse events expand? Does the dosing burden change? Do dose-optimization studies support long-term use?Only when all these questions are answered in the affirmative can a multi-target design be considered a meaningful advancement.

 3. The advantage of small molecules such as JAK inhibitors is their adjustability; their risks stem from their broader mode of action

 JAK inhibitors are the fastest-acting class of drugs for treating autoimmune skin diseases, but their broader mechanism of action also means there are more potential sources of risk. Clinicians should evaluate JAK inhibitors by balancing their rapid onset of action, convenience of oral administration, and dose adjustability against risks such as infections, laboratory abnormalities, drug interactions, and long-term safety.The risk evidence for different JAK molecules (JAK1/JAK2/JAK3/TYK2) and different indications (rheumatoid arthritis, psoriasis, atopic dermatitis, alopecia areata, vitiligo) must be evaluated separately; a one-size-fits-all approach is not appropriate.

 3.1 The convenience of oral administration is meaningful only when patients can manage their treatment long-term

 The greatest advantage of JAK inhibitors is oral administration; patients do not require injections, resulting in naturally higher adherence. However, “convenience of oral administration” is only a superficial advantage; whether long-term management is truly feasible depends on dosing frequency, monitoring requirements, restrictions on concomitant medications, pregnancy planning, use in elderly patients, and management of patients with comorbidities. Convenience should not obscure the costs associated with screening, follow-up, and risk communication.

 Regarding dosing frequency: for upatitinib, the maintenance dose for response-related dermatitis is 15 mg or 30 mg once daily; for abuxitinib, 100 mg or 200 mg once daily; for baretinib, 2 mg or 4 mg once daily; for tofacitinib, 5 mg twice daily or 11 mg once daily as an extended-release tablet; and for degositinib, once daily. Most JAK inhibitors are administered once daily, offering high convenience.However, this convenience comes with monitoring requirements: all JAK inhibitors require baseline screening for tuberculosis, hepatitis B, hepatitis C, and HIV; during treatment, regular monitoring of complete blood count (every 2–4 weeks for the first 3 months, then every 1–3 months), liver function (monthly for the first 3 months, then every 3 months), and lipid profile (every 1–3 months) is required. In the long term, this monitoring burden is no less significant than that of biologics.

 Table 3-1 Comparison of Dosage and Monitoring Requirements for JAK Inhibitors

Drug	Dosage Frequency	Baseline Screening	Monitoring During Treatment	Special Notes
Tofatinib	5 mg twice daily or 11 mg once daily (extended-release)	Tuberculosis/Hepatitis B/Hepatitis C/HIV	Complete blood count / Liver and kidney function / Lipid profile / Blood pressure	Use with caution in patients aged 50 and older with cardiovascular risk
Barretinib	2 mg or 4 mg once daily	Same as above	Same as above	Monitor for VTE risk
Upatinib	15 mg or 30 mg once daily	Same as above	Same as above	Monitor for acne and HSV
Abuxitinib	100 mg or 200 mg once daily	Same as above	Same as above	For severe, refractory AD, the dose may be increased to 200 mg
Degositinib	Once daily	Same as above	Same as above	Phase III data are available for alopecia areata
Deuterated brutinib	Once daily	Same as above	Same as above	Selective TYK2 inhibitor with superior long-term safety

 Regarding drug interactions, dose adjustment is required when JAK inhibitors are used in combination with strong CYP3A4 inhibitors (such as ketoconazole and clarithromycin);concomitant use with immunosuppressants (e.g., methotrexate, azathioprine, cyclosporine) increases the risk of infection and bone marrow suppression; concomitant use with live vaccines is contraindicated; and concomitant use with anticoagulants requires monitoring for bleeding risk. Biologics have fewer restrictions in this regard, and the record of drug-drug interactions is relatively clear.

 Regarding pregnancy planning, JAK inhibitors are currently not recommended for use during pregnancy, while trying to conceive, or during lactation, as animal studies have shown teratogenicity (embryo-fetal toxicity); treatment should be discontinued at least 4 weeks prior to conception (specific durations may vary slightly by drug).Among biologics, TNF inhibitors (particularly pecelizumab) have a good safety profile during pregnancy and are minimally transferred across the placenta; safety data for IL-17, IL-23, and IL-4/13 inhibitors during pregnancy are limited, and discontinuation is generally recommended during the second and third trimesters.

 Table 3-2 Precautions for the Use of JAK Inhibitors in Special Populations

Population	Recommendations	Alternative Options	Key Monitoring Points
Pregnant Women	Not recommended; discontinue use at least 4 weeks before pregnancy	Pexelizumab (if a biologic is required)	Pregnancy Test
Breastfeeding Women	Not recommended	Individual assessment Biologics	Infant monitoring
Elderly (≥65 years)	Use tofacitinib with caution; consider JAK-1 selective	IL-23 inhibitors or usulizumab	Cardiovascular Events
Patients with concomitant cardiovascular risk	Avoid tofacitinib	JAK-1 selective inhibitors or biologics	MACE/VTE
Concomitant diabetes	May be used; requires monitoring of blood glucose and infection	Biologics may be preferable	Infection monitoring
History of cancer	Use with caution; refer to ORAL Surveillance data	Biologics or non-immunosuppressive regimens	Tumor Monitoring
Latent tuberculosis	May be used following preventive antituberculosis therapy	Same as above	Active tuberculosis
Hepatitis B carrier	May be used after prophylactic antiviral therapy	Same as above	HBV reactivation

 In elderly patients (≥65 years) with concomitant cardiovascular risk factors (hypertension, diabetes, hyperlipidemia, history of smoking, or prior cardiovascular events), the ORAL Surveillance trial of tofacitinib demonstrated higher rates of MACE and malignancies compared to the TNF inhibitor control group;Tofalitinib should be used with caution in these patients; more selective JAK1 inhibitors (upatitinib, abuxitinib, degositinib) or biologics may be considered. Patients with active or latent tuberculosis must complete preventive antituberculosis therapy before using JAK inhibitors; HBV carriers require prophylactic antiviral therapy (e.g., entecavir, tenofovir).

 Table 3-3 Comparison of Oral Convenience and Management Costs

Dimension	Apparent Advantages	Hidden Costs	Net Benefit Assessment
Route of Administration	Oral administration; no injections required	Requires frequent laboratory monitoring	Depends on access to monitoring
Onset of Action	Takes 1–2 weeks to take effect	Must be initiated after baseline screening	Requires advance planning
Dose adjustment	Dosage is adjustable	Dose adjustments require monitoring support	Monitoring capabilities are required
Special Populations	Approval has been granted for certain indications in children	Numerous restrictions for pregnant women, the elderly, and patients with comorbidities	Requires individual assessment
Long-term use	May have higher adherence	Long-term safety data remain limited	Long-term events require monitoring

 Recommendations: The convenience of oral administration of JAK inhibitors is a genuine advantage, but this advantage can only be realized if patients can complete baseline screening, long-term monitoring, management of concomitant medications, and exclusion of specific patient populations. Before prescribing JAK inhibitors, clinicians should assess patients’ access to monitoring, comorbidities, pregnancy plans, and cardiovascular risk, and avoid equating “convenience of oral administration” with “ease of management.”

 3.2 Selectivity Must Be Demonstrated by Clinical Data, Not Molecular Labels

 The JAK family comprises four members: JAK1, JAK2, JAK3, and TYK2, each of which plays a distinct role in signaling pathways: JAK1 mediates signaling for various cytokines such as IL-6, IFN, and IL-2; JAK2 primarily mediates signaling for hematopoietic factors such as EPO, TPO, and GM-CSF; inhibition of JAK2 leads to anemia and neutropenia;JAK3 mediates signaling of γc-family cytokines such as IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21; TYK2 mediates signaling of IFN-α, IL-12, and IL-23. Different JAK inhibitors exhibit distinct selectivity profiles; whether these differences in “molecular labels” truly translate into differences in clinical safety requires validation by clinical data.

 Table 3-4: Selectivity of the JAK Family and Clinical Implications

JAK Member	Primary Signaling Pathways Mediated	Potential Effects of Inhibition	Representative Drugs
JAK1	IL-6, IFN, IL-2	Immunosuppression, risk of infection	Upatinib, Abciximab, Degositinib
JAK2	EPO, TPO, GM-CSF	Anemia, neutropenia	Barretinib (partial inhibition)
JAK3	γc-family cytokines	Immunosuppression, risk of infection	Tofatinib (partial inhibition)
TYK2	IFN-α, IL-12, IL-23	Superior efficacy in psoriasis and better long-term safety	Deuterated brutinib

 Tofalitinib inhibits JAK1/JAK3 (with some inhibition of JAK2 as well); baricitinib inhibits JAK1/JAK2; upalitinib selectively inhibits JAK1; abuxitinib selectively inhibits JAK1; degositinib selectively inhibits JAK1; deuterated brutinib selectively inhibits TYK2 (already approved by the FDA for psoriasis).In vitro selectivity data are derived from enzymatic and cellular assays, reflecting molecular-level preferences; in vivo selectivity must be assessed based on actual target occupancy (e.g., differences in phosphorylated STAT inhibition between JAK1 and JAK2 in patients’ peripheral blood cells), efficacy within the dose range, and the profile of adverse events.

 In atopic dermatitis, there were significant differences in efficacy and adverse event rates between the 15 mg and 30 mg dose groups for upatitinib: the 30 mg group showed slightly better efficacy, but had slightly higher rates of acne, headaches, HSV infections, and venous thromboembolic events.These dose-effect and dose-toxicity relationships reflect true selectivity more accurately than molecular labeling. Since deuterated brutinib selectively inhibits TYK2, it theoretically avoids JAK1/JAK2-related adverse events; signals for MACE and malignancies at the ORAL Surveillance level have not yet been observed among TYK2 inhibitors, but long-term data still need to be accumulated.

 Table 3-5: Levels of Evidence for Selectivity

Level of Evidence	Type	Credibility	Clinical Translation
1	In vitro Enzymatic Selectivity	Basic Data	Reflects preferences at the molecular level only
2	In vitro cellular selectivity	Basic Data	Reflects preferences at the cellular level
3	In vivo Target Occupancy	Moderate	Reflects actual inhibition in patients
4	Dose-response relationship	High	Reflects true selectivity within the clinical dose range
5	Dose-Toxicity Relationship	High	Reflects true safety within the clinical dose range
6	Positive control head-to-head	High	Reflects the true difference compared to the control
7	Long-term safety extension study	Highest	Reflects the true risk associated with long-term use

 Cross-trial comparisons are another pitfall in the evaluation of JAK inhibitors.Patient baselines (disease duration, prior treatments, comorbidities), endpoint definitions (EASI 75 vs. EASI 90 vs. vIGA-AD 0/1), follow-up duration (12 weeks vs. 16 weeks), and control group designs (placebo vs. active control) vary across trials; directly comparing remission rates would lead to erroneous conclusions.The Heads Up trial of upatitinib (head-to-head with dupilumab) showed that the proportion of patients achieving EASI 90 in the upatitinib group was significantly higher than in the dupilumab group at week 16; however, longer-term data are still needed to determine whether this difference persists through week 52 and whether it is associated with a higher rate of adverse events.The POETYK PSO series of trials with deuterated brepitinib showed a PASI 75 rate of approximately 58%–59% (at Week 16) in psoriasis, which is lower than that of existing IL-23 inhibitors and IL-17 inhibitors, but it exhibits greater selectivity and superior long-term safety data.

 Table 3-6: Pitfalls and Solutions in Cross-Trial Comparisons

Comparison Dimensions	Common Pitfalls	Countermeasures
Patient Baseline	Differences in disease duration, prior treatment, or comorbidities	Subgroup Analysis or IPD Meta-Analysis
Endpoint Definition	EASI 75 vs. 90 vs. vIGA-AD 0/1	Unified endpoints or MAIC adjustment
Duration of follow-up	12 weeks vs. 16 weeks vs. 52 weeks	Comparison at the Same Time Point
Control group	Placebo vs. Active Control	Network meta-analysis or head-to-head comparison
Adverse Events	Differences in definitions and reporting criteria	Standardized AE collection
Special populations	Differences in Inclusion and Exclusion Criteria	Subgroup Analysis

 Recommendations: When evaluating JAK inhibitors, clinicians should consider the following: molecular selectivity profile, actual target occupancy data, efficacy-toxicity relationships across the dose range, head-to-head data from positive-control trials (if available), long-term safety extension studies, and data from special populations. Relying solely on the “JAK1 selectivity” or “TYK2 selectivity” stated on the molecular label is insufficient to determine the true risk-benefit ratio in clinical practice.

 4. The real issue with non-oncological ADCs is whether they can selectively eliminate pathogenic cells

Over the past decade, ADCs (Antibody-Drug Conjugates) have primarily advanced in the field of cancer treatment, with traditional single-target ADCs (such as trastuzumab-metanxin conjugates, vibrotuximab, and goserotuzumab, which target HER2, EGFR, and TROP2, respectively) receiving successive approvals for use in hematologic malignancies and solid tumors.However, industry indicators suggest that the enthusiasm surrounding traditional single-target ADCs in terms of transactions and R&D has cooled to a more rational level over the past two years, with bispecific ADCs and “non-oncology” ADCs (i.e., the use of ADC toxin payloads for the treatment of autoimmune diseases) emerging as new focal points of attention.

 As an academic conference focused on dermatology and venereology, EADV 2026 is not the primary arena for ADC technology; however, the expansion of ADC technology from oncology to immune-mediated diseases may offer new insights for the treatment of autoimmune skin diseases. It is important to note that the use of ADCs in the treatment of autoimmune skin diseases is currently in the early exploratory stages and lacks formal clinical data from EADV. This article analyzes it as a “cross-disciplinary trend signal” rather than an established category of dermatological treatment.

 4.1 From Tumor Killing to Immune Modulation: The Definition of the Therapeutic Window Will Change

 The design logic behind tumor ADCs is as follows: antibodies target antigens on the surface of tumor cells, enabling the directed delivery of cytotoxic payloads (such as microtubule inhibitors or DNA-damaging agents like MMAE, MMAF, DM1, and DXd) to tumor cells to achieve selective killing. The therapeutic window is determined by the gap between “cytotoxicity against tumor cells” and “toxicity to normal tissues.”Patients with advanced-stage cancer have a limited life expectancy and a higher tolerance for toxicity, so the therapeutic window can be narrower.

 The design logic for ADCs targeting autoimmune diseases may be entirely different.In cutaneous autoimmune diseases (such as SLE, dermatomyositis, psoriasis, atopic dermatitis, hidradenitis suppurativa, and vitiligo), the pathogenic cells are typically abnormally activated immune cell subsets (such as Th17, Tfh, B cells, plasma cells, and ILC2), which also play physiological roles in healthy individuals; “complete elimination” of these cells could lead to unacceptable immunodeficiency.Patients with autoimmune diseases may undergo treatment for years or even decades, and their tolerance for cumulative toxicity is far lower than that of patients with advanced cancer; therefore, the therapeutic window must be significantly wider than that of tumor ADCs.

 Table 4-1 Comparison of Therapeutic Windows for Tumor ADCs and Immune ADCs

Dimension	Tumor ADCs	Immune ADCs (Exploratory Directions)
Target Cells	Tumor Cells (Abnormal Proliferation)	Pathogenic Immune Cell Subpopulations (Physiological Functions)
Elimination Strategy	Complete Elimination	Elimination or Temporary Modulation
Payload type	Highly toxic microtubule inhibitors/DNA-damaging agents	Immunomodulators/Low-toxicity functional payloads
Treatment Duration	Several months to several years (depending on remission)	Possibly several years or even decades
Tolerance to toxicity	High (patients with advanced cancer)	Low (patients with chronic diseases)
Therapeutic window requirements	May be narrow	Must be significantly wide
Concerns regarding cumulative toxicity	Relatively minor	Core concern
Bystander effect	Helps kill heterogeneous tumors	May damage healthy tissue

 Payload selection is a central issue in the design of immune ADCs. The highly toxic microtubule inhibitors (MMAE, MMAF) and DNA-damaging agents (DXd, PBD) commonly used in tumor ADCs may not be suitable for immune diseases: while eliminating pathogenic cells, they may damage healthy bystander cells, leading to long-term immune suppression.Directions currently being explored for payloads in immune ADCs include “functional payloads” such as immunomodulators (e.g., glucocorticoid receptor agonists, dexamethasone derivatives), IL-2 mutants, TLR agonists, JAK inhibitor payloads, and Bcl-6 inhibitors, with the aim of temporarily modulating rather than permanently eliminating pathogenic cells.This concept of “modulatory payloads” is fundamentally different from the “killer payload” logic used in anti-tumor ADCs.

 Table 4-2 List of ADC Payload Types

Payload Type	Mechanism of Action	Applicable Scenarios	Risks
MMAE/MMAF	Microtubule inhibition	Tumor ADCs	Bystander effect, neurotoxicity
DM1/DM4	Microtubule inhibition	Tumor ADC	Hepatotoxicity
DXd	Topoisomerase I Inhibition	Oncological ADC	Myelosuppression
PBD	DNA cross-linking	Tumor ADCs	High toxicity
Glucocorticoid derivatives	Immunomodulation	Immune ADC Research	Systemic glucocorticoid effects
JAK Inhibitor Payload	JAK pathway inhibition	Exploration of Immunotherapy ADCs	Immunosuppression
IL-2 Mutants	Treg Expansion	Immune ADC Exploration	Off-target effects
TLR agonists	Immune modulation	Immune ADC Exploration	Inflammatory Response

 The bystander effect is another core issue in ADC design. After a cleavable linker releases its payload within a target cell, the payload can diffuse through the cell membrane to adjacent cells, killing bystander cells that do not express the target antigen; in contrast, a non-cleavable linker releases its payload only within the target cell, resulting in a weaker bystander effect.In tumor ADCs, the bystander effect helps kill heterogeneous tumor cells; in immunotherapy ADCs, however, the bystander effect may damage healthy tissue cells (such as skin keratinocytes, fibroblasts, and endothelial cells), requiring more careful linker design.

 Table 4-3: Impact of the bystander effect in different types of ADCs

ADC Type	Linker Selection	Bystander Effect	Clinical Significance
Tumor-Targeting ADCs (Heterogeneous)	Cleavable	Helps eliminate heterogeneous tumors	Improves therapeutic efficacy
Tumor ADC (Homogeneous)	Non-cleavable	Limited bystander effect	Reduces off-target toxicity
Immune ADCs (clearance-type)	Cleavable or non-cleavable	May damage healthy cells	Requires careful evaluation
Immune ADC (modulatory)	Preference for non-cleavable	Bystander effects should be minimized	Reduce off-target effects

 Recommendations: When evaluating immunological ADCs, R&D teams should ask the following questions: Is there sufficient expression difference between target cells in diseased and healthy tissues? Is the payload’s cytotoxicity appropriate for the immune-mediated disease? Is the goal to eliminate diseased cells or to temporarily modulate them? Could the bystander effect harm normal cells? What is the expected duration of treatment for patients, and is the cumulative toxicity acceptable? Until official data from the EADV is available, these questions should serve only as research directions and not as the basis for clinical decision-making.

 4.2 Dual-target approaches may enhance selectivity but may also increase manufacturing and interpretation challenges

The design logic behind bispecific antibody-drug conjugates (ADCs) is to use a bispecific antibody to simultaneously target two tumor-associated antigens (or two different epitopes of the same antigen), thereby widening the therapeutic window by enhancing selectivity and improving endocytosis efficiency.Industry indicators suggest that Chinese pharmaceutical companies hold a significant leading edge in the field of bispecific antibody-drug conjugates (ADCs), with multinational giants continuing to acquire global rights to Chinese bispecific ADC pipelines through substantial upfront payments. However, whether a “dual-target” approach truly enhances selectivity depends on the specific design logic behind the dual-target strategy.

 The logic behind dual-target design can be divided into three categories: first, complementary recognition (where the two targets are expressed at different levels on pathogenic cells and healthy cells, respectively; simultaneous binding to both targets triggers endocytosis, thereby increasing selectivity for pathogenic cells); second, synergistic endocytosis (where simultaneous binding to both targets triggers more efficient receptor-mediated endocytosis, improving payload delivery efficiency);third, expanded binding scope (binding occurs when either of the two targets is expressed, broadening therapeutic coverage but potentially reducing selectivity). These three logics must be validated separately: do they improve pathogenic cell recognition, enhance endocytosis, or merely expand the binding scope?

 Table 4-4 Classification of Dual-Target Design Logics and Validation Requirements

Design Logic	Mechanism	Expected Benefits	Potential Risks	Validation Requirements
Complementary Recognition	Endocytosis is triggered only when both targets bind simultaneously	Enhanced selectivity for pathogenic cells	Some pathogenic cells may express only a single target, potentially leading to detection gaps	Target Co-expression Profile
Synergistic endocytosis	Binding to both targets enhances endocytosis efficiency	Improved payload delivery	Excessive endocytosis may increase toxicity	Endocytosis kinetics
Expanding the Binding Range	Binding occurs when either target is expressed	Expanded Therapeutic Coverage	Selectivity may decrease	Tissue Distribution Data

 Manufacturing complexity is a real challenge for bispecific ADCs. The production of bispecific antibodies is more complex than that of monoclonal antibodies, requiring solutions to issues such as heavy-chain-to-heavy-chain mismatches and heavy-chain-to-light-chain mismatches. Commonly used technologies include KiH (Knobs-into-Holes), CrossMab, DVD-Ig, and Wuxibody.Conjugation uniformity (DAR distribution, Drug-to-Antibody Ratio) is more difficult to control than in monoclonal antibody-based ADCs, and the design of conjugation sites for bispecific antibody-based ADCs (cysteine conjugation, lysine conjugation, non-natural amino acid conjugation, and enzyme-catalyzed conjugation) requires more precise process optimization.The stability of the linker must exhibit a distinct difference between plasma and target cells; otherwise, premature release of the payload in plasma could lead to off-target toxicity.

 Table 4-5 List of Key Quality Attributes (CQAs) for Bispecific Antibody-Drug Conjugates (ADCs)

CQA	Test Method	Acceptance Criteria Reference	Impact
DAR Distribution	HIC-HPLC, LC-MS	Main peak ≥ 70%	Efficacy-Toxicity Balance
Binding Sites	Peptide map, LC-MS	Site specificity ≥ 95%	Homogeneity
Free Payload	SEC-HPLC, RP-HPLC	≤2%	Safety
Unconjugated Antibodies	HIC-HPLC	≤10%	Competitive binding
Aggregated Antibodies	SEC-HPLC	≤5%	Immunogenicity
Fragment Antibodies	CE-SDS	≤5%	Stability
Linker Plasma Stability	Plasma Incubation LC-MS	48-hour release ≤5%	Non-targeted toxicity
Endocytic Release Efficiency	Cell-based assays	≥70%	Efficacy

 Table 4-6 Protection Requirements for Highly Active Loads (OEB Levels 4/5)

Protection Dimensions	Requirements	Engineering Implementation
Production Environment	OEB Class 4/5 Isolator	Negative-pressure, sealed system
Operators	Air-supplied protective suits	Self-contained breathing apparatus
Wastewater Treatment	Dedicated treatment facilities	Activated Carbon Adsorption + Incineration
Exhaust Gas Treatment	Dedicated exhaust system	HEPA Filtration
Analytical Methods	High-Sensitivity LC-MS/MS	Detection at the ng/mL level
Transport and Storage	Dedicated containers and temperature control	Cold chain + isolation

 Impurity profiles include unconjugated antibodies, free payload, aggregated antibodies, and antibody fragments; each type of impurity may affect safety and efficacy. Batch-to-batch consistency is a core metric for commercial production, and the comparability between clinical and commercial batches requires rigorous validation.Protection requirements for highly reactive payloads (OEB Class 4/5, such as MMAE, PBD, DXd, etc.) represent another challenge in ADC production, requiring specialized engineering capabilities—a new challenge for both small-molecule oral drug manufacturers and monoclonal antibody manufacturers.

 Action Recommendations: When evaluating bispecific ADC projects, R&D and business development (BD) teams should verify the following: Is the dual-target design logic clear? Has it been experimentally validated? What is the conjugation uniformity (DAR distribution) like? Are the linker stability data complete? Is the impurity profile clear? Do the batch-to-batch consistency data cover both clinical and commercial batches? Are safeguards for highly active payloads in place? These factors determine whether a project can truly advance to clinical trials and commercialization—rather than merely being labeled a “bispecific ADC” in transaction news.

 4.3 Skin Diseases Offer a Sampling Advantage, but Reliable Efficacy Biomarkers Are Still Needed

 Skin diseases offer an advantage in translational research that diseases affecting other organs cannot match: sample accessibility.Skin lesions can be directly biopsied for a variety of studies, including histopathological evaluation, immunohistochemistry, flow cytometry, single-cell sequencing, and spatial transcriptomics; peripheral blood samples can be paired with tissue samples to investigate the correlation between circulating biomarkers and tissue changes; and paired pre- and post-treatment biopsies can establish a causal chain linking “molecular changes—cellular changes—clinical improvement.”

 This accessibility makes skin diseases an ideal setting for the early clinical validation of immunotherapy ADCs. In Phase I or IIa trials, paired pre- and post-treatment biopsies allow for direct observation of the following: Has the number of target cells decreased? Is the extent of this reduction synchronized with clinical symptom improvement? Have bystander cells been damaged? Does the distribution of the payload within the tissue align with expectations? Have pharmacodynamic markers changed?The answers to these questions provide a more accurate reflection of the drug’s true mechanism of action than clinical endpoints alone (such as PASI or EASI).

 Table 4-7: List of Sampling Advantages for Skin Diseases

Advantage Dimensions	Specific Content	Applications in Translational Research
Tissue Accessibility	Direct sampling from skin lesion biopsies	Pathology, IHC, flow cytometry, single-cell sequencing
Pre- and post-treatment paired samples	Biopsies from the same patient at different time points	Establishing a Molecular-Cellular-Clinical Causal Chain
Peripheral Blood Pairing	Blood-Tissue Pairing	Validation of Circulating Biomarkers
Reproducible Imaging	Dermoscopy, Reflective Confocal Microscopy	Dynamic assessment of lesion changes
Quantifiable symptoms	Itch NRS, Pain NRS	Correlation with histological changes
PRO data available	Quality of life, work productivity	Correlation with biomarkers

 However, developing efficacy biomarkers is no simple task. A reliable efficacy biomarker must meet the following criteria: it must be measurable in the affected tissue; it must correlate with the number or activity of target cells; it must correlate with clinical symptom improvement; it must be reproducible across different patients; it must show changes early in treatment (e.g., within 1–2 weeks); and it must correlate with long-term outcomes (e.g., maintenance of remission).Commonly used potential effectrator markers include: Th17 cell proportion, IL-17A/IL-22 expression levels, IL-23/IL-12p40 expression, keratinocyte proliferation markers (Ki67), T-cell activation markers (HLA-DR, CD25),B-cell and plasma cell markers (CD19, CD20, CD138), and type I IFN signaling markers (IFIT1, MX1), among others. Each marker requires independent validation.

 Table 4-8 List of Candidate Efficacy Markers for Immunological ADCs

Marker	Cell Type	Assay Method	Validation Status
Th17 Proportion	Th17 Cells	Flow cytometry, IHC	Partially validated for psoriasis
IL-17A/IL-22	Th17 cells	qPCR, IHC	Partially validated for psoriasis
IL-23/IL-12p40	Dendritic cells	qPCR, IHC	Validated for psoriasis
Ki67	Keratinocytes	IHC	Validated
HLA-DR/CD25	T cells	Flow cytometry, IHC	Validated
CD19/CD20/CD138	B cells/plasma cells	Flow cytometry, IHC	Partially validated for SLE
IFIT1/MX1	Type I IFN signaling	qPCR, IHC	Validated for SLE
Tfh proportion	Tfh cells	Flow cytometry	Under investigation

 The causal relationship between short-term tissue changes and long-term disease modification requires further validation over a longer period. The fact that an immunotherapy ADC reduces Th17 cells in skin lesions by 70% within 4 weeks does not necessarily mean that the drug can sustain disease remission for 5 years;The rebound kinetics of Th17 cells, compensatory mechanisms by other cell subsets, and the re-establishment of immune memory may all influence long-term outcomes. Clinical study designs should include extended follow-up (at least 52 weeks), post-discontinuation follow-up, and re-treatment assessments following relapse to fully characterize the relationship between efficacy biomarkers and clinical outcomes.

 Table 4-9 Validation of Causal Chains Between Short-Term Tissue Changes and Long-Term Disease Modification

Validation Dimensions	Short-Term Trials	Extension-phase follow-up	Validation Requirements
Target Cell Reduction	Visible within 4–12 weeks	Maintenance or rebound	Requires dynamic assessment
Improvement in clinical symptoms	Occurs concurrently with cytopenia	Whether sustained	Requires PRO assessment
Bystander cell damage	Assessed concurrently	Whether recovery occurs	Requires histological evaluation
Changes in pharmacodynamic markers	May change early on	Predict long-term outcomes	Requires correlation analysis
Response Duration	Not evaluated	Median duration of remission after discontinuation	Requires discontinuation—follow-up
Response to re-treatment	Not evaluated	Still effective	Requires a re-treatment substudy

 Recommendations: When evaluating immunomodulatory ADCs, translational research teams should prioritize skin diseases that allow for tissue sampling as early clinical settings; include paired pre- and post-treatment biopsies in Phase I/II trials; simultaneously develop efficacy biomarkers at both the tissue and peripheral blood levels; conduct correlation analyses between changes in efficacy biomarkers and improvements in clinical endpoints; and establish long-term follow-up cohorts to validate the relationship between short-term tissue changes and long-term outcomes.These efforts better reflect the true value of the project than rushing to expand indications.

 5. From bio europe fall 2026 to EADV: The Boom in China’s Bispecific Antibody-ADC Transactions Does Not Substitute for Immuno-Dermatological Applicability

 Industry signals indicate that Chinese pharmaceutical companies are active in bispecific antibody-drug conjugate (ADC) R&D and business development (BD) transactions, while multinational corporations (MNCs) continue to acquire global rights to Chinese bispecific ADC pipelines through substantial upfront payments. This BD fervor reflects the oncology sector’s recognition of bispecific ADC technology; however, transactions involving oncology assets cannot be equated with clinical needs in dermatology and immunology. The fact that a technology platform attracts attention from MNCs does not necessarily mean it has been validated for non-oncology indications. This pattern—where platform hype outpaces indication fit—has become a defining signal for biotech licensing deals.

 5.1 BD Teams Should Examine Indication Logic Before Platform Labels

 A common bias among BD teams when evaluating bispecific ADC projects is to first focus on platform labels (“bispecific ADC,” “leading in China”) and then consider the indication rationale. This sequence can easily lead to the high-priced acquisition of projects that are meaningful in the oncology field but lack relevance to the company’s own therapeutic areas. The correct sequence should be to first evaluate the indication rationale, followed by the platform labels. Such deals are a familiar failure mode in pharma M&A—one that BD teams should consciously avoid.

 The checklist for evaluating indication logic includes: Is there causal evidence for the target in human disease (genetic evidence, animal models, clinical intervention evidence)? Is the patient population large enough to support clinical development and commercialization? What are the efficacy and safety profiles of existing standard-of-care treatments, and can the new drug provide meaningful improvements? What is the acceptable level of risk for patients and physicians? How long will the validation cycle take (early-stage clinical trials → Phase II → Phase III → approval)?These questions determine whether a project is worth further evaluation, while the platform label merely indicates the project’s “background.”

 Table 5-1 BD Evaluation Checklist—Prioritizing Indication Logic

Evaluation Dimensions	Question	Data Sources	Evaluation Criteria
Causal Evidence for the Target	Is there causal evidence for the target in human diseases?	Genetics/Animal Models/Clinical Interventions	Supported by at least two types of evidence
Patient Population Size	What is the size of the target patient population?	Epidemiological data	sufficient to support clinical development
Existing Standard of Care	Efficacy and safety of existing treatments?	Guidelines/Real-world data	Unmet medical needs exist
Risk Acceptability	What level of risk is acceptable to patients and physicians?	Patient Preference Studies	Equivalent to or better than existing treatments
Validation Cycle	How long does it take from early-stage clinical trials to approval?	Development History of Similar Drugs	Alignment with Company Strategy
Commercial potential	Projected Post-Launch Sales?	Market Research	Recoupability of R&D Investment
Competitive Landscape	Number of Competitors Targeting the Same Target/Mechanism?	ClinicalTrials.gov	Ample Room for Differentiation

 Early-stage deal valuations can reflect the level of competition for a project but do not prove the ultimate value of the product. A deal with an upfront payment of $500 million reflects the buyer’s optimistic expectations for the project in a specific indication; however, it will take years—or even decades—to verify whether the project can meet its primary endpoints in Phase III trials, obtain regulatory approval, secure health insurance coverage after launch, and demonstrate clinical value in the real world.Historically, there have been numerous cases of high-value business development deals that ultimately failed: projects with promising early-stage data that failed in Phase III trials, those with post-approval sales far below expectations, or those in which serious adverse events were discovered after market launch.

 Table 5-2: Discrepancy Between Early-Stage Transaction Values and Final Product Value

Stage	Transaction Value Reflects	Potential Deviation	Validation Point
Initial Payment	Buyer’s Optimistic Expectations for the Project	Risk of Phase III failure	3–5 years from now
Milestone Payment	Expected Development Progress	Risk of Regulatory Rejection	5–8 years later
Post-Launch Sales	Commercialization Expectations	Sales Below Expectations	10 years later
Long-term safety	Safety Database Projections	Rare Adverse Events	10–15 years later

 The differences between oncology asset development and clinical needs in dermatology and immunology must be clearly defined. The core objective of oncology ADCs is to kill tumor cells, so a narrow therapeutic window is acceptable; the core objective of dermatology and immunology ADCs is to modulate pathogenic cells, so the therapeutic window must be significantly wider than that of oncology ADCs. Oncology patients have a high tolerance for toxicity, whereas dermatology and immunology patients have a low tolerance for toxicity. Oncology treatment typically lasts from several months to several years (depending on remission), while dermatology and immunology treatment may last for decades.These differences dictate that the design requirements for the same ADC platform are entirely different across these two indications, and transfer between indications requires revalidation.

 Table 5-3: Distinctions in Clinical Requirements Between Oncology and Dermatological Immunology

Dimension	Oncology ADC Requirements	Dermatological ADC Requirements	Differences
Target Cells	Tumor Cells (Elimination)	Pathogenic Immune Cells (Elimination or Modulation)	Immune cells have physiological functions
Therapeutic Window	May be narrow	Must be wide	Variations in toxicity tolerance
Treatment duration	Several months to several years	Possibly decades	Differences in cumulative toxicity
Payload Type	Highly toxic, lethal	Regulatory-type preferred	Different mechanisms
Monitoring Requirements	Relatively centralized	Long-term monitoring	Differences in Management Costs
Access to Health Insurance	Good Coverage for Cancer	Significant disparities in health insurance coverage for chronic diseases	Differing Economic Requirements

 Action Recommendations: When evaluating bispecific antibody and ADC projects, the BD team should prioritize verifying the following: causal evidence for the target within the company’s own indications; patient population size and the current therapeutic landscape; acceptable risk levels; validation timelines and costs; and synergy with the company’s existing pipeline. Acquiring a project at a high price solely because its platform has attracted attention from multinational corporations (MNCs) may result in acquiring a project that is meaningful in the oncology field but irrelevant to the company’s own indications.

 5.2 Cross-indication platform reuse must undergo revalidation

 “Platform reuse” is a common term in the ADC field, meaning that the same combination of antibody, linker, and payload can be reused across different indications, saving development costs and time. However, platform consistency does not equate to product comparability—the actual performance of the same platform across different indications may vary significantly, and each component must be validated separately to determine its suitability for the new indication.

 Assessment of antibody component reuse: Are the expression patterns of the antibody’s target similar on tumor cells and immune cells? Is the endocytosis efficiency comparable? Is the affinity suitable for the new indication (tumor ADCs often require high affinity to ensure cell killing, while immune ADCs may require moderate affinity to avoid excessive clearance)? Do the effector functions of the antibody’s FC region (ADCC, CDC, ADCP) need to be silenced (to avoid triggering additional inflammation in immune diseases)?These questions determine whether the same antibody requires engineering modifications for cross-indication use.

 Table 5-4 Checklist for Evaluating ADC Component Reuse—Antibody

Evaluation Dimensions	Oncology ADC Requirements	Immune ADC Requirements	Feasibility of Reuse
Target Expression Pattern	High Expression in Tumors	High expression in pathogenic cells, low expression in healthy cells	Requires Re-evaluation
Endocytosis Efficiency	High (ensures cell killing)	Moderate (to avoid excessive clearance)	May require adjustment
Affinity	High (nM range)	Moderate (may need to be reduced)	May require engineering
FC Effect Function	Preserved (enhances cytotoxicity)	Silenced (to prevent inflammation)	Requires engineering
Immunogenicity	Acceptable	Lower levels required (for long-term use)	Humanization required

 Reusability assessment of the linker subcomponent: Is the linker’s stability in plasma suitable for long-term administration in autoimmune diseases (where the dosing interval for immune ADCs may be longer than for oncology ADCs)? Is the linker’s release mechanism within target cells still effective? Does the linker’s chemical structure cleave normally within the intracellular environment of immune cells? Does the linker’s immunogenicity differ in patients with this new indication?

 Reusability Assessment of the Payload Component: Is the payload’s mechanism of action suitable for autoimmune diseases (cytotoxic payloads such as MMAE may not be suitable, while modulatory payloads such as glucocorticoids and JAK inhibitors are more likely to be suitable)?Does the potency of the payload need to be adjusted (immunological diseases may require lower potency to avoid excessive clearance)? Is the bystander effect of the payload acceptable in the new indication? Do the metabolism and excretion of the payload differ in patients with immunological diseases?

 Table 5-5 Checklist for Evaluating ADC Component Reuse—Linker and Payload

Component	Requirements for Oncology ADCs	Immune ADC Requirements	Reusability Feasibility
Ligand Plasma Stability	≤5% release over 48 hours	May require a longer period (72 hours+)	Re-evaluation required
Conjugate Release Mechanism	Cleavable or non-cleavable	Non-cleavable may be preferred	Requires reselection
Ligand immunogenicity	Acceptable	Needs to be lower	Needs evaluation
Mechanism of action of the payload	Cytotoxic	Regulatory-type preferred	Typically requires replacement
Load Effectiveness	High (pM range)	Medium to low (nM level)	Requires adjustment
Load spectator effect	Acceptable	Should be minimized	Requires redesign
Load Metabolism	Hepatic/renal excretion	May vary	Re-evaluation required

 Re-evaluation of the reuse of dose and efficacy assays: Does the dose range need to be redefined for immune diseases (typically requiring a lower starting dose)? Are the efficacy assay methods (e.g., cytotoxicity assays, target binding assays) still appropriate for the new indication (efficacy assay methods for regulatory payloads differ from those for cytotoxic payloads)? Does the correlation between clinical pharmacokinetics and pharmacodynamics need to be re-established?

 Table 5-6 Gaps in Platform Consistency and Product Comparability

Dimension	Platform Consistency	Product Comparability	Source of Discrepancy
Antibodies	Same Antibody Sequence	Performance may vary across different indications	Differences in Target Expression and Endocytosis
Linker	Same chemical structure	Stability requirements may differ	Differences in dosing intervals
Payload	Same payload	Suitability may differ	Differences in mechanism of action requirements
Dose	Same dosage range	Usually requires readjustment	Differences in toxicity tolerance
Efficacy Testing	Same method	A new method may be required	Differences in load type
PK/PD	Same Correlation	Must be re-established	Differences in Patient Populations

 Recommendations: When evaluating the reuse of a platform across indications, the R&D team should separately assess the suitability of each component—antibody, linker, payload, dose, and potency assay—for the new indication.The antibody may require engineering modifications to the FC region; the linker may require longer plasma stability; the payload may need to be switched from a cytotoxic to a modulatory type; the dosage may need to be redefined; and the potency assay may need to be redeveloped. Only by thoroughly completing these tasks can one determine whether “platform reuse” truly accelerates development or is merely a marketing label.

 6. Different Attendees Should Use Different Questions to Screen EADV Data Before and After bio europe fall 2026

 The EADV 2026 program spans clinical, translational, and industrial dimensions, and attendees with different roles come to Vienna with distinct objectives: clinicians focus on whether the findings can change patient management; translational researchers focus on subtyping and organizational evidence; and R&D and BD teams focus on differentiation, long-term safety, and manufacturing feasibility. Merging all attendees’ focus areas into a single, unified “attendee itinerary” would result in a generic list of participants that offers no practical assistance for actual attendance.This chapter breaks down the program by role, listing the key issues each role should prioritize. For BD teams, EADV’s clinical signals also inform the business development forum that defines the autumn biotech circuit.

 6.1 Clinical Teams Should Prioritize Long-Term Control and Patient Burden

 The core task for clinicians at EADV 2026 is to determine: Which new data might change my treatment plan for patients next Monday? This question sounds simple, but when actually screening abstracts, it’s easy to be misled by labels such as “new mechanism” or “new target.” Clinical teams should prioritize the following dimensions: remission durability, relapse and rescue therapy, infections and monitoring, and patient-reported outcomes.

 Response Duration: What is the follow-up duration of the trial? What are the sustained response rates at 12 weeks, 16 weeks, 52 weeks, 3 years, and 5 years, respectively? Is the definition of sustained response reasonable (PASI 90 vs. vIGA 0/1)? Do dose-optimization studies report sustained response rates for different maintenance doses? These data determine the drug’s true value in long-term management.

 Relapse and Rescue Therapy: What is the median time to relapse after discontinuation? Is retreatment effective following a relapse? What are the rescue therapy options (re-initiation of the original drug, switching to other targets, or combination therapy)? Does repeated discontinuation and retreatment affect immunogenicity? These data determine the drug’s suitability for intermittent treatment strategies.

 Infections and Monitoring: What is the incidence of serious infections? What are the risks of herpes zoster, tuberculosis reactivation, and opportunistic infections? What is the frequency and scope of laboratory monitoring? These data determine the safety management burden associated with long-term use of the drug.

 Patient-Reported Outcomes: Are PROs reported as co-primary or secondary endpoints? Do improvements in scores such as the Itch NRS, DLQI, POEM, and WPAI reach the minimum clinically important difference (MCID)? Is the improvement in PROs synchronized with the improvement in lesion scores? These data determine whether the drug truly improves patient experience, rather than merely the appearance of skin lesions.

 Table 6-1 Clinical Team EADV Data Screening Checklist

Dimension	Question	Data Source	Assessment Criteria
Duration of Remission	Follow-up Duration and Proportion of Sustained Responders?	Trial Design/Extension Studies	Data on sustained response at ≥52 weeks
Relapse and Rescue	Median time to relapse after discontinuation? Response to retreatment?	Discontinuation-to-Follow-Up Substudy	Median time to relapse ≥ 12 weeks
Infections and Monitoring	Incidence of severe infections? Monitoring frequency?	Safety Database	Equivalent to current treatments
Improvement in PROs	Were PROs reported? Was the MCID met?	Secondary Endpoints	Itch NRS improvement ≥4 points
Special populations	Data on the elderly, children, or patients with comorbidities?	Subgroup analysis	Data available for specific populations
Real-world	Are there any real-world studies?	RWE Poster	Consistent with trial results

 When conference abstracts are insufficient to drive guideline updates, the maturity of the evidence should be clearly stated. Most reports at EADV 2026 consist of Phase II trial data or real-world studies, with limited Phase III trial data and even fewer long-term safety extension studies. Clinicians should distinguish between: which data are sufficient to change clinical practice (e.g., positive Phase III results + long-term safety data + approved indication updates)?Which data merely indicate a development signal (e.g., positive Phase II results, still awaiting Phase III validation)? Which data remain hypothetical (e.g., mechanism-of-action studies, translational research)?

 Action Recommendations: Prior to EADV 2026, clinical teams should compile a list of “difficult-to-treat patients” encountered in outpatient clinics this month (e.g., psoriasis with poor response to IL-17 inhibitors, atopic dermatitis with waning response to dupilumab, hidradenitis suppurativa complicated by tuberculosis) and use these specific questions to search for relevant data during the conference;During the conference, record abstracts according to the four dimensions of “sustained remission—relapse—infection—PRO”; after the conference, classify conclusions into three categories: “may impact practice,” “provides signals for development,” and “remains hypothetical.”

 6.2 The translational team should first identify the differences between responders and non-responders

 The core task for translational researchers at EADV 2026 is to identify the differences between “responders” and “non-responders,” providing clues for future patient stratification and biomarker development. While this task may seem straightforward, it is easy to fall into the trap of “explaining only the best responders” in practice. Failed cases often hold greater explanatory value than successful ones—only by understanding why treatment failed can patients be properly selected for the next round of trials.

 Sampling Timepoints: Does the trial include paired biopsy samples collected before treatment, during treatment (e.g., at 1 week, 4 weeks, 12 weeks), and after treatment? Are the sample collection timepoints aligned with clinical assessment timepoints? Is the sample processing method (frozen vs. formalin-fixed) suitable for subsequent multiplex immunohistochemistry, single-cell sequencing, and spatial transcriptomics?

 Differences Between Tissue and Peripheral Blood: Are changes in biomarkers at the tissue level (e.g., reduced Th17 cells in skin lesions) correlated with levels in peripheral blood (e.g., peripheral blood Th17 cell proportion, serum IL-17A levels)? Can peripheral blood biomarkers replace tissue biomarkers in clinical practice?

 Biomarker Thresholds: Were the biomarker thresholds predefined? Were the thresholds validated in an independent cohort? Do the thresholds remain valid across different patient subgroups (e.g., different ethnicities, disease severity, and prior treatments)?

 Failure Samples: Were samples from non-responders retained in the trial? What are the tissue and peripheral blood characteristics of non-responders? Do non-responders share common predictive features (e.g., high baseline type I IFN signaling, specific HLA types, specific microbiome characteristics)? Failure samples often provide greater interpretive value than success samples—only by understanding why treatment failed can patients be properly selected for the next round of trials.

 Table 6-2: EADV Data Screening Checklist for Translational Teams

Dimension	Question	Data Source	Evaluation Criteria
Sample Time Point	Is the biopsy paired? Are the time points aligned?	Trial Design	Paired before/during/after treatment
Tissue vs. Peripheral Blood	Correlation between tissue and peripheral blood?	Analysis of paired samples	r ≥ 0.6
Biomarker Threshold	Is the threshold preset? Has it been validated?	Statistical Analysis	Independent Cohort Validation
Failed samples	Are non-responders included?	Sample Bank	Analysis of Failed Samples
Mechanism Hypotheses	Is there any mechanism research?	Basic Research	Consistent with clinical data
Single-cell/spatial omics	Is single-cell/spatial omics used?	Omics data	Cell-type resolution

 Action Recommendations: The translational team should preemptively compile a list of target biomarkers and mechanistic hypotheses prior to EADV 2026; during the conference, evaluate abstracts based on the four dimensions of “sample time point—differences between tissue and peripheral blood—biomarker thresholds—failure samples”; after the conference, share data with the clinical and R&D teams to determine which biomarkers warrant inclusion in the patient stratification design for the next round of clinical trials.

 6.3 R&D and BD Teams Should First Determine Whether the Therapeutic Window Can Be Expanded

 The core task for the R&D and BD teams at EADV 2026 is to determine which new molecules or platforms warrant the company’s investment of resources. This assessment must comprehensively evaluate the depth of efficacy, scope of action, toxicity, dosing frequency, manufacturability, and competitive landscape—rather than focusing solely on short-term remission rates or platform labels.

 Depth of Efficacy: Does the new molecule’s remission rate (PASI 90, EASI 90, etc.) outperform existing standard of care? Does it demonstrate superiority across the entire patient population, or only in specific subgroups (e.g., refractory or comorbid cases)? Is the depth of remission accompanied by improvements in Patient-Reported Outcomes (PROs)?

 Scope of Action: What is the scope of the new molecule’s indications? Is it a single-indication drug or a platform molecule (capable of covering multiple indications)? Is there sufficient clinical evidence for cross-indication use? Does an expansion of the scope of action entail an expansion of the toxicity profile?

 Toxicity: How does the adverse event profile of the new molecule compare to that of existing standard treatments? Is the incidence of serious adverse events comparable? Is there sufficient long-term safety data? Is there adequate safety data for special populations (the elderly, pregnant women, patients with renal impairment, and patients with hepatic impairment)?

 Dosage Frequency: What is the dosage frequency during the maintenance phase? Is the route of administration (subcutaneous injection, oral, intravenous infusion) convenient for patients? How does dosage frequency relate to the maintenance of remission?

 Manufacturing Feasibility: Is the production process for the molecule mature? Are the data on conjugation uniformity, batch-to-batch consistency, impurity profiles, and stability complete for bispecific antibodies, ADCs, and multifunctional molecules? Are the containment requirements for highly active payloads manageable?

 Competitive Landscape: How many competing products are in development targeting the same target or mechanism? What are the market share and health insurance coverage of already marketed products? Is there sufficient room for differentiation to support commercialization?

 Table 6-3: EADV Data Screening Checklist for R&D and BD Teams

Dimension	Question	Data Source	Evaluation Criteria
Efficacy Depth	Is the remission rate superior to that of existing treatments?	Primary Endpoint of the Trial	Superiority or non-inferiority + safety advantage
Scope of Action	Scope of Indications?	Pipeline Planning	Prioritize platform-based molecules
Toxicity	What is the profile of adverse events?	Safety Database	Equivalent to or better than existing treatments
Dosage Frequency	Frequency during the maintenance phase?	Dosage regimen	Equivalent or superior convenience
Manufacturing feasibility	Is the process mature?	CMC data	Acceptable batch-to-batch consistency
Competitive Landscape	Number of Competitors? Differentiation?	ClinicalTrials.gov	Ample room for differentiation
CMC Consistency	Analytical methods and batch-to-batch consistency for complex molecules?	CMC Documentation	CQA Batch-to-Batch Variability Is Acceptable

 For complex molecules (bispecific antibodies, ADCs, multifunctional molecules), there is particular scrutiny regarding analytical methods and batch-to-batch consistency. Analytical methods for complex molecules form the foundation for evaluating product quality and include SEC-HPLC, CE-SDS, ICIEF, LC-MS, and others; batch-to-batch consistency data must cover clinical batches, process validation batches, and commercial batches, and batch-to-batch variation in Critical Quality Attributes (CQAs) should fall within acceptable limits.Focusing solely on efficacy data while ignoring CMC data may result in acquiring a project with an immature process that cannot be commercialized.

 Action Recommendations: Prior to EADV 2026, the R&D and BD teams should outline the company’s pipeline strategy and differentiation positioning; during the conference, evaluate new molecules based on the six dimensions of “efficacy depth—scope of action—toxicity—dosage frequency—manufacturing feasibility—competitive landscape”; after the conference, classify projects into three categories—“priority advancement,” “continued observation,” and “not currently under consideration”—and conduct additional CMC due diligence for complex molecular projects.

 7. Maintain clear boundaries for evidence before and after the conference

 As an academic conference, EADV 2026’s abstracts, oral presentations, and poster content all constitute “public conference materials,” but the level of evidence varies by content type. Conference abstracts may contain preliminary data from unpublished Phase II trials; oral presentations may present data from Phase III trials that have been submitted but not yet published; and posters may feature exploratory analyses or mechanism-of-action studies. It is essential to maintain clear boundaries regarding the level of evidence both before and after the conference to avoid equating conference data with validated clinical evidence.

 7.1 Use Qualifying Language for Non-Oncology ADCs

 There may be no formal clinical data reports on non-oncology ADCs at EADV 2026, and related discussions may be limited to satellite sessions, industry forums, or informal exchanges. In the absence of formal EADV abstracts or clinical data to support them, the potential of non-oncology ADCs in the treatment of dermatological conditions should be described using language indicating that further validation is required, rather than definitive language.

 List of “to be validated” language: Use “may offer new avenues” rather than “is set to transform the treatment of skin diseases”; use “warrants further observation” rather than “holds great promise”; use “requires validation” rather than “has been proven”; use “is being explored” rather than “has become a trend”; use “theoretically possible” rather than “will certainly be realized.”

 Table 7-1 List of “To Be Verified” Language—Non-Oncology ADCs

Assertive Expressions (Avoid)	Phrases Requiring Validation (Recommended)	Usage Scenarios
Set to revolutionize the treatment of skin diseases	May Offer New Approaches	Describes potential
Promising Prospects	Worth Watching	Describing Progress
Already Proven	Needs verification	Evidence Description
Has become a trend	Under exploration	Describes the direction
Will definitely be realized	Theoretically possible	Describes the mechanism
Disruptive breakthrough	New Research Approach	Describing innovation
Revolutionary progress	Areas Worth Watching	Describing Progress

 This linguistic standard is a fundamental requirement of scientific writing. Presenting unverified hypotheses as verified facts misleads readers and undermines the author’s academic credibility. In actual reports from EADV 2026, authors should clearly distinguish between: which data are from official conference abstracts; which are unofficial information released by companies; and which are the authors’ own analyses and speculations. The sources and credibility of each category of information differ.

 Recommendations: When writing conference reports or review articles related to EADV 2026, clearly label the non-oncology ADC sections with the statement “Currently, there are no official EADV clinical data to support this,” and use language indicating that the related discussions are subject to verification; for data from official conference abstracts, specify the abstract number, presentation type (oral/poster), study design (Phase I/II/III, real-world), follow-up duration, and primary endpoint;for unofficial information released by companies, cite the source (company website, press release, investor conference).

 7.2 Use Original Sources for Specific Transactions and Project Status

 While industry signals mentioning the activity of Chinese pharmaceutical companies in bispecific ADC transactions constitute industry background information, specific data such as transaction amounts, project stages, target information, and approval statuses must be verified against primary sources. Secondary sources (industry media reports, social media comments, analyst reports) are prone to data distortion, outdated information, or misrepresentations.

 List of primary sources: Company announcements (announcements from publicly traded companies, press releases on company websites, investor relations pages); clinical trial registrations (ClinicalTrials.gov, China Clinical Trials Registry (ChiCTR), European Union Clinical Trials Register (EU CTR)); conference abstracts (official abstract releases from conferences such as EADV, ASCO, AACR, ESMO, etc.); regulatory documents (approval documents, labeling, and treatment guidelines from the FDA, EMA, and NMPA);academic journals (peer-reviewed research articles).

 Table 7-2 Source Verification Checklist—Transaction and Project Status

Information Type	Original Source	Credibility	Update Frequency
Transaction Amount	Listed Company Announcements/Company Website	Highest	Real-time
Project Stage	ClinicalTrials.gov/Company Announcements	High	Weekly
Target Information	Conference Abstracts/Scientific Papers	High	Monthly
Approval Status	FDA/EMA/NMPA Official Websites	Highest	Real-time
Trial Design	ClinicalTrials.gov	High	Weekly
Safety Data	Regulatory Documents/Academic Papers	High	Monthly
Market Sales	Company Financial Reports	High	Quarterly

 Verification Dimensions: Transaction Amount (Initial Payment, Milestone Payments, Total Transaction Amount, Equity Investment Ratio);Project Phase (Preclinical, Phase I, Phase II, Phase III, Approved, Post-Marketing); Target Information (Target Name, Target Type, Bispecific Antibody Logic); Indications (Approved Indications, Investigational Indications, Discontinued Indications); Approval Status (Approving Country, Approval Date, Approval Conditions, Post-Marketing Commitments).

 Table 7-3 Transaction and Project Status Verification Dimensions

Dimension	Verification Points	Common Errors
Transaction Amount	Down Payment vs. Total Transaction Amount	Entering the down payment as the total transaction amount
Project Phase	Phase I/II/III/Approved	Listing Phase II as Phase III
Target Information	Target Name/Type/Bispecific Antibody Rationale	Change “under investigation” to “approved”
Indications	Approved vs. In Development vs. Discontinued	Change “Discontinued” to “In Development”
Approval Status	Country/Date/Conditions	List items that were withdrawn after going on sale as “Currently Available”
Scope of Equity	Global vs. Regional	List regional rights as “Global”

 Avoiding the copying of amounts, development stages, or approval statuses from secondary sources is a fundamental requirement of scientific writing and industry analysis. Common errors in secondary sources include: misreporting an upfront payment as the total transaction amount; misclassifying a Phase II trial as Phase III; describing a target currently under investigation as an approved target; and referring to a drug withdrawn from the market as a drug currently on the market. These errors can significantly impact readers’ assessment of a project.

 Action Recommendations: When writing conference reports or industry analyses related to EADV 2026, prioritize verifying original sources for content involving specific transaction amounts, project phases, target information, and approval statuses;Secondary sources should be used only as leads, not as final references; after verification, cite the information sources in the text (e.g., “According to the company’s announcement on X, X, 2025,” “According to ClinicalTrials.gov registration number NCT0XXXXXX”); double-check the information before formal publication to avoid outdated data.

 8. Conclusion: The Next Wave of Value in Cutaneous Immunotherapy Lies in Narrower Scope of Action and Longer-Lasting, Reliable Control

 The focus of EADV 2026 has shifted from “whether there are new drugs” to “whether treatment is sufficiently precise.” Over the past decade, treatment options for autoimmune skin diseases have expanded significantly due to the successive launches of biologics and small molecules such as JAK inhibitors; however, an increase in options does not automatically equate to improved treatment quality. The next set of questions that dermatologists and R&D teams need to address centers more on how to improve treatment precision rather than continuing to expand the number of targets.True progress lies in delivering sufficient, reversible, or manageable interventions to the right patients, the right cells, and within the right time window—rather than simply suppressing the immune system more aggressively.

 Now that biologics have entered a phase of mature competition, patient stratification is more important than adding new targets. Drugs targeting IL-17, IL-23, IL-12/23, IL-4/13, TSLP, and other targets are already on the market, and the differences in efficacy between drugs within the same class are narrowing; future progress lies in identifying which patients are best suited for which drug, which patients can achieve deep remission, and which patients are prone to relapse.Post-discontinuation performance, dose optimization, response to retreatment, and management of special patient populations better reflect a drug’s long-term value than short-term remission rates.

 The advantages of small molecules such as JAK inhibitors include adjustability, the convenience of oral administration, and rapid onset of action; however, their broader mechanisms of action also imply a greater number of potential risks. Differences in selectivity among different JAK molecules (JAK1, JAK2, JAK3, TYK2) must be demonstrated by clinical data rather than molecular labels; safety management for elderly patients with concomitant cardiovascular risk is a key consideration in the use of JAK inhibitors; and the monitoring burden and restrictions on concomitant medications should not be overshadowed by the “convenience of oral administration.”

 Table 8-1 Comparison of Core Characteristics Across Three Pathways in Cutaneous Immunotherapy

Dimension	Biologics (Monoclonal Antibodies)	JAK Small Molecules	Non-Oncology ADCs (Exploratory Direction)
Mechanism of Action	Blocking a Single Signaling Pathway	Inhibition of JAK signaling	Targeted elimination/regulation of pathogenic cells
Onset of Action	2–4 weeks	1–2 weeks	Unknown
Duration of Remission	Varies widely (longer for IL-23)	Relapse 4–8 weeks after discontinuation	Unknown
Route of administration	Subcutaneous injection	Oral	Intravenous infusion (presumed)
Selectivity	Route selectivity	Molecular selectivity (to be clinically validated)	Cellular selectivity (to be verified)
Monitoring Burden	Relatively low	High (complete blood count/liver and kidney function/lipid profile)	Unknown
Reversibility	Reversible	Reversible	Irreversible in the clearance type; reversible in the regulatory type
Level of Evidence	Mature (multiple products approved)	Partially mature (several approved)	Early-stage exploration

 The real challenge posed by non-oncology ADCs is whether they can selectively eliminate or modulate pathogenic cells. Shifting from tumor killing to immune modulation requires a fundamental redefinition of the therapeutic window: patients with immune-mediated diseases have a much lower tolerance for cumulative toxicity than those with advanced cancer, necessitating a reassessment of payload selection, bystander effects, linker stability, and the design logic behind dual-target approaches.The transaction momentum surrounding Chinese bispecific ADCs does not equate to their applicability in dermatological immunology; platform consistency does not imply product comparability, and cross-indication reuse must be revalidated. Until formal clinical data are released at EADV 2026, the potential of non-oncology ADCs in the treatment of skin diseases remains a “research direction awaiting validation” rather than a “mature therapeutic category.”

 Different attendees arrived in Vienna with different questions: clinical teams prioritized long-term control and patient burden; translational teams focused on distinguishing responders from non-responders; and R&D and BD teams sought to determine whether the therapeutic window could be expanded. Breaking down the conference itinerary by role offers more practical value than a generic “conference guide.” Both before and after the conference, maintain clear boundaries of evidence, use “to be validated” language regarding non-oncology ADCs, and verify specific transactions and project statuses against original sources.

 Table 8-2: List of Core Questions for Different Attendees at EADV 2026

Attendee Role	Core Issues	Priority Data	Next Steps
Clinicians	Can patient management be changed?	Long-term control/patient burden	Update Treatment Regimens
Translational Researchers	What distinguishes responders from non-responders?	Biomarkers/Tissue Evidence	Designing a stratified study
R&D Team	Can the therapeutic window be expanded?	Efficacy-Toxicity/CMC	Advance or Terminate the Project
BD Team	Is the Project Worth Acquiring?	Indications Logic/Platform Label	Due Diligence or Withdrawal
Medical Affairs	How Is Data Communicated to Physicians?	Key Endpoints/Safety Data	Preparing Educational Materials
Regulatory Affairs	What Indications Are Supported by the Data?	Trial Design/Endpoints	Preparing Regulatory Communications

 The next wave of value in cutaneous immunotherapy stems from a narrower scope of action and longer-lasting, reliable control.True progress lies in implementing sufficient, reversible, or manageable interventions for the right patients, with the right cells, and within the right time window—rather than in stronger immunosuppression. While concrete data at EADV 2026 may offer only partial clues regarding this direction, embracing this approach better reflects the true value of clinical practice and R&D than chasing every new target and molecular label.

 Recommendations for Action: Before and after the EADV 2026 conference, clinicians, translational researchers, and R&D and business development (BD) teams should screen data with specific questions in mind to avoid being misled by labels such as “new mechanisms” or “new targets”; distinguish between the three levels of evidence maturity—“may impact practice,” “provides a signal for development,” and “remains hypothetical”; maintain the boundaries of the evidence in conference reports and industry analyses, use language indicating that findings are “to be verified,” and cross-check with original sources;and conduct a comprehensive assessment that incorporates long-term control, patient burden, manufacturing feasibility, and the competitive landscape, rather than focusing solely on short-term remission rates.

 9. EADV Congress 2026 Frequently Asked Questions

 This section answers frequently asked questions related to the EADV Congress 2026 and the field of cutaneous immunotherapy, helping readers at obtain accurate and concise information. All answers are based on the EADV official website and publicly available academic materials; please double-check venue and schedule updates before the official release.

 9.1 When and Where Will the EADV Congress 2026 Be Held?

 The EADV Congress 2026 (the 35th Congress of the European Academy of Dermatology and Venereology) will take place from September 30 to October 3, 2026, in Vienna, Austria. The official conference website is https://eadv.org/. The specific venue, detailed schedule, and registration procedures are subject to the final notice released by the EADV prior to the conference.

 As the capital of Austria, Vienna is one of Europe’s leading academic hubs for dermatology and venereology and has hosted the EADV Annual Congress on multiple occasions. The Austria Center Vienna is one of Europe’s largest conference centers and is equipped to host major international academic conferences. Please refer to the information officially released by the EADV for specific venue arrangements.

9.2 What Immunotherapy Trends Should Be Watched at EADV 2026

 The immunotherapy areas worth watching at EADV 2026 primarily include the following categories:

 ① Large-molecule biologics (monoclonal antibodies) for autoimmune diseases: These include IL-17 inhibitors (secukinumab, eculizumab, brolizumab), IL-23 inhibitors (guselkumab, risatumab, teclizumab),IL-12/23 inhibitors (usnumab), IL-4/13 inhibitors (duplixent), and TSLP inhibitors (tezolizumab), among others, with new data on their use in psoriasis, atopic dermatitis, hidradenitis suppurativa, prurigo nodularis, vitiligo, and other conditions.

 ② Oral small-molecule drugs such as JAK inhibitors: Long-term safety data, management data for special populations, and data on the expansion of new indications for JAK inhibitors—including tofacitinib, baricitinib, upatitinib, abuxitinib, degositinib, and deuterated bricitinib—in autoimmune skin diseases.

 ③ New Directions in Immunotherapy: These include non-oncology ADCs (exploratory approaches using ADC toxin payloads or regulatory payloads for autoimmune diseases), bispecific antibodies, multifunctional molecules, and novel immunomodulators.

 Note: The application of non-oncology ADCs in the treatment of skin diseases remains an emerging cross-disciplinary trend; there are currently no formal clinical data from the EADV to support this, and it should be treated as a “research direction worth monitoring” rather than an “established therapeutic category.”

 9.3 How Should Biologics and Small Molecules Be Compared?

 Comparisons between biologics and small molecules such as JAK inhibitors should be based on multiple dimensions rather than a simple ranking of advantages and disadvantages. The specific comparison dimensions are as follows:

 ① Onset of action: JAK inhibitors typically take effect within 1–2 weeks, while biologics usually take 2–4 weeks to take effect.

 ② Remission maintenance: Remission can be maintained for up to 28–48 weeks after discontinuation of IL-23 inhibitors; with IL-17 inhibitors, relapse typically occurs 12–16 weeks after discontinuation; and with JAK inhibitors, relapse occurs 4–8 weeks after discontinuation.

 ③ Administration: Biologics are administered via subcutaneous injection (once monthly to once every 12 weeks), while JAK inhibitors are taken orally (once or twice daily).

 ④ Dosage flexibility: JAK inhibitors allow for dose adjustment (e.g., upatilinib 15 mg vs. 30 mg), whereas biologics offer limited scope for dose adjustment.

 ⑤ Safety Monitoring: JAK inhibitors require routine monitoring of complete blood count, liver and kidney function, and lipid levels; biologics typically require only baseline screening for tuberculosis, hepatitis B, and hepatitis C, followed by periodic follow-up.

 ⑥ Comorbidities and Patient Preferences: JAK inhibitors (especially tofacitinib) should be used with caution in elderly patients with concomitant cardiovascular risk factors; JAK inhibitors and most biologics are generally avoided in pregnant women; patients who prefer oral medication may choose JAK inhibitors, while those who prefer longer intervals between injections may opt for IL-23 inhibitors or usulizumab.

 Rather than attempting a simple “which is better” ranking, the most appropriate treatment regimen should be selected based on the patient’s specific circumstances (age, comorbidities, prior treatment, pregnancy plans, and personal preferences).

 Table 9-1 Summary of Comparison Criteria Between Biologics and JAK Small Molecules

Dimension	Biologics	JAK Inhibitors	Selection Tendencies
Onset of Action	2–4 weeks	1–2 weeks	Choose JAK for urgent onset of action
Relief Maintenance	IL-23 takes longer	Rapid relapse after discontinuation	Choose IL-23 for long-term maintenance
Administration method	Subcutaneous injection	Oral	If oral administration is preferred, choose a JAK inhibitor
Adjustability	Low	Higher	Choose JAK if flexible dose adjustment is required
Safety Monitoring	Relatively low	High	Poor monitoring accessibility; choose biologics
Cardiovascular Risk	Relatively low	Tofacitinib: Higher	Combined risk: Choose a biologic
Pregnancy planning	Partially available	Avoid	Choose a biologic when planning pregnancy
Children	Partially Approved	Partially approved	Select Based on Indications

 Recommendation: When selecting biologics or JAK inhibitors for patients, clinicians should comprehensively consider six factors—onset of action, remission maintenance, administration route, dose adjustability, safety monitoring, and comorbidities—along with patient preferences, and engage in shared decision-making with patients, rather than simply relying on labels such as “newer drugs are better” or “oral administration is more convenient.”