IMMUNOGENICITY OF GUSELKUMAB AMONG PSORIASIS PATIENTS IN VOYAGE 1&2 STUDIES
Kristian Reich,1 April W. Armstrong,2 Yaowei Zhu,3 Megan Miller,3 Yin You,3 Yaung-Kaung Shen,3 Ya-Wen Yang,4 Peter Foley,5 Christopher E. M. Griffiths,6 Bruce Strober 7
1Translational Research in Inflammatory Skin Diseases, Institute for Health Services Research in Dermatology and Nursing, University Medical Center Hamburg-Eppendorf, Germany; 2Keck School of Medicine, University of Southern California, Los Angeles, CA, USA; 3Janssen 
Research & Development, LLC, Spring House, PA, USA; 4Immunology Global Medical Affairs, Janssen Pharmaceutical Companies of Johnson & Johnson, Horsham, PA, USA; 5University of Melbourne, St. Vincent’s Hospital Melbourne and Probity Medical Research, Skin Health 
Institute, Carlton, VIC, Australia; 6Dermatology Centre, Salford Royal Hospital, University of Manchester, Manchester, UK; 7Yale University, New Haven, CT, USA and Central Connecticut Dermatology Research, Cromwell, CT, USA 

  BACKGROUND/OBJECTIVE METHODS CONCLUSIONS

This poster was supported by Janssen Research & Development, LLC • Originally Presented at EADV’s 30th Congress, Virtual, September 29-October 2, 2021. Presented at The Winter Clinical Dermatology Conference - Hawaii® (WC22), 14th-19th JAN 2022.

• VOYAGE 1 & 2 were phase 3, randomized, double-blinded, 
placebo- and active comparator-controlled studies of 
guselkumab (GUS) in adult patients with moderate-to-
severe plaque psoriasis1,2

• The development of anti-drug antibodies (ADA) to 
biologic agents is a normal immune response but may 
affect efficacy and/or safety3

• Here, we assessed the association between the 
development of ADA to GUS and either the extent of 
clinical response or incidence of injection-site reactions 
(ISRs) through 5 years in the VOYAGE 1 and VOYAGE 2 
studies

• Of all GUS-treated patients with evaluable samples, 14.4% (111/770) in VOYAGE 1 and 15.5% (146/943) in VOYAGE 2 were positive 
for ADA through Week 264

• In both studies, ADA titres were predominantly low, with 82.0% in VOYAGE 1 and 82.2% in VOYAGE 2 having  peak titres ≤1:160

• Only 5 (4.5%) and 8 (5.5%) ADA positive patients in VOYAGE 1 and VOYAGE 2, respectively, were positive for NAbs to GUS

• Through the end of the 5-year VOYAGE 1 and VOYAGE 2 studies of 
GUS in psoriasis, 15% of patients had developed ADA to GUS. Of 
these, 5% had antibodies that were classified as neutralizing, which 
equates to 0.8% of all GUS-treated patients.

• The development of ADA (or NAb) was not associated with 
either reduced clinical efficacy or increased ISR rates. However, 
these data should be interpreted with caution due to the limited 
number of patients developing ADA/NAb and/or experiencing 
ISRs within 5 years of commencing treatment.

 METHODS (CONT'D) RESULTS

DBL, database lock; PE, primary endpoint; R, randomization; SE, secondary endpoint; q2w, every 2 weeks; q8w, every 8 weeks.
*The last dose of guselkumab was administered at Week 252; efficacy was evaluated through Week 252. 
†Safety was evaluated through Week 264.

DBL, database lock; Nonresponders [NR] <PASI 90; PASI, Psoriasis Area and Severity Index; PE, primary endpoint; R, randomization; SE, secondary endpoint; 
Responders [R] ≥PASI 90; q2w, every 2 weeks; q8w, every 8 weeks.
*Upon loss of ≥50% of improvement in PASI achieved at Week 28 or at Week 72 if prerequisite loss of PASI improvement was not observed, then reinitiate or 
initiate guselkumab.
†The last dose of guselkumab was administered at Week 252; efficacy was evaluated through Week 252. 
‡Safety was evaluated through Week 264. 

Disclosures References
1. Blauvelt A, et al. J Am Acad Dermatol. 2017;76(3):405-17.

2. Reich K, et al. J Am Acad Dermatol. 2017;76(3):418-31.

3. Tsakok T, et al.  J Eur Acad Dermatol Venereol. 2021;35(2):329-37.

Figure 1. VOYAGE 1 Study Design

Figure 2. VOYAGE 2 Study Design

Kristian Reich – served as advisor and/ or paid speaker for and/or participated in clinical trials sponsored by AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Forward Pharma, Galderma, Gilead, Janssen-Cilag, Kyowa Kirin, Leo, Medac, Novartis, Ocean Pharma, Pfizer, Sanofi, UCB, co-founder of MoonLake Immunotherapeutics. April W. Armstrong - research investigator and/or scientific advisor to AbbVie, Boehringer Ingelheim, BMS, 
Dermavant, Dermira, EPI Health, Incyte, Janssen, KHK, Leo, Lilly, Modmed, Novartis, Ortho Dermatologics, Pfizer, Regeneron, Sanofi, Sun, and UCB. Peter Foley - received grant support from AbbVie, Amgen, Celgene, Janssen, Leo Pharma, Lilly, Merck, Novartis, Pfizer, Sanofi, and Sun Pharma. He has served as an investigator for AbbVie, Akaal, Amgen, Arcutis, Argenx, Aslan, AstraZeneca, BMS, Boehringer Ingelheim, Botanix, Celgene, Celtaxsys, CSL, Cutanea, Dermira, Galderma, 
Genentech, GSK, Hexima, Janssen, Leo Pharma, Lilly, MedImmune, Melaseq/Geneseq, Merck, Novartis, Pfizer, Regeneron Pharmaceuticals Inc, Reistone, Roche, Sanofi, Sun Pharma, Teva, UCB Pharma, and Valeant, He has served on advisory boards for AbbVie, Amgen, BMS, Boehringer Ingelheim, Celgene, Galderma, GSK, Janssen, Leo Pharma, Lilly, Mayne Pharma, Merck, Novartis, Pfizer, Sanofi, Sun Pharma, UCB Pharma, and Valeant. He has served as a consultant for 
BMS, Galderma, GenesisCare, Janssen, Leo Pharma, Lilly, Mayne Pharma, MedImmune, Novartis, Pfizer, Roche, UCB Pharma, and Wintermute. He has received travel grants from AbbVie, Galderma, Janssen, Leo Pharma, Lilly, Merck, Novartis, Pfizer, Roche, Sun Pharma, and Sanofi, and has served as a speaker for or received honoraria from AbbVie, Amgen, Celgene, Galderma, GSK, Janssen, Leo Pharma, Lilly, Merck, Novartis, Pfizer, Roche, Sanofi, Sun Pharma, and Valeant.  
Christopher E. M. Griffiths - received honoraria as an advisory board member and/or speaker from AbbVie, Almirall, Bristol Myers Squibb, Eli Lilly, Galderma, Janssen, Leo, Novartis, Pfizer, Sun Pharma, and UCB Pharma and research grants from AbbVie, Celgene, Eli Lilly, Janssen, Leo, Novartis, Pfizer, and Sandoz. Bruce Strober - received honoraria or research grants as a consultant, speaker, and/or investigator for AbbVie, Almirall, Amgen, Arcutis, Arena, Aristea, Boehringer 
Ingelheim, Bristol Myers Squibb, Cara, Celgene, Dermavant, Dermira, Equillium, GlaxoSmithKline, Janssen, Leo, Eli Lilly, Meiji Seika Pharma, Mindera, Novartis, Ortho Dermatologics, Pfizer, Sanofi-Genzyme Sun Pharma, Regeneron, and UCB Pharma; as scientific director for the CorEvitas Psoriasis Registry; and as Editor-in-Chief at the Journal of Psoriasis and Psoriatic Arthritis. Yaowei Zhu, Megan Miller, Yin You, and Yaung-Kaung Shen are all employees of Janssen Research & 
Development, LLC; and Ya-Wen Yang is an employee of Janssen Immunology Global Medical Affairs; employees may own stock in Johnson & Johnson, of which Janssen is a subsidiary..

• VOYAGE 1 and VOYAGE 2 were identical through Week 24; patients were randomized at baseline as follows 
(Figures 1 and 2):

 o GUS 100 mg administered by subcutaneous (SC) injection at Weeks 0, 4, and 12, then every 8 weeks (q8w) 
 o Placebo at Weeks 0, 4, and 12, followed by GUS 100 mg SC at Weeks 16 and 20, then q8w 
 o Adalimumab 80 mg SC at Week 0, 40 mg at Week 1, then 40 mg every 2 weeks (q2w) through Week 23

• In VOYAGE 1 (Figure 1), patients in the adalimumab group continued on adalimumab 40 mg q2w through 
Week 47 and crossed over to receive GUS at Week 52. All patients entered the open-label GUS treatment 
period during Weeks 52-252.

• In VOYAGE 2 (Figure 2), patients entered a randomized withdrawal and retreatment period from Week 28  
to 72. Patients entered the open-label GUS treatment period during Weeks 76-252.

• Venous blood samples were collected at regular visits for the detection of antibodies to GUS. The ADA were 
detected using a validated electrochemiluminescence immunoassay (ECLIA) method.

• The incidence and titres of ADA to GUS were summarized through Week 264 for all patients who were 
treated with at least one dose of GUS and had evaluable serum samples following treatment

• If a patient had a positive sample at the reference baseline visit, the patient was considered as positive only 
if the peak titre of the post-GUS treatment samples was ≥2-fold higher than that of the reference sample at 
baseline

• Serum samples that tested positive for ADA to GUS were further characterized to determine if the antibodies 
that had developed could neutralize the biologic activity of GUS in vitro (i.e., neutralizing antibodies [NAbs] 
to GUS)

• The proportions of patients achieving clinical response at Week 252 were evaluated by positive/negative 
ADA status

• Clinical response was defined as achieving ≥90% improvement in the Psoriasis Area and Severity Index (nearly 
complete clearance; PASI 90) or 100% improvement (complete clearance; PASI 100) and as an Investigator’s 
Global Assessment (IGA) score of 0/1 (cleared or minimal) or 0 (cleared)

• The proportions of patients experiencing ISRs through Week 264 were evaluated by positive/negative  
ADA status

Active-comparator Period

Guselkumab
(n=329)

Placebo
(n=174)

Adalimumab
(n=334)

Guselkumab 100 mg at Weeks 0 and 4, then q8w

Adalimumab 80 mg at Week 0, 40 mg at Week 1, then q2w

Weeks 0 4 16
PE
SE

24
SE

48
SE

52 252* 264†

5 Year
DBL

Guselkumab 100 mg at Weeks 16 
and 20, then q8w

Guselkumab 100 mg at Week 52, then q8w

Placebo

Placebo-
crossover

Placebo-
controlled

Open-label

Guselkumab
(n=496)

Placebo
(n=248)

Adalimumab
(n=248)

Guselkumab 100 mg at 
Weeks 0 and 4, then q8w

Initiate guselkumab 100 mg Weeks 28 and 32, 
then q8w

Placebo withdrawal → guselkumab treatment upon 
loss of responses*

Placebo withdrawal → guselkumab retreatment upon 
loss of responses*

Placebo withdrawal → guselkumab retreatment upon 
loss of responses*

Continue guselkumab 100 mg q8w 

Continue guselkumab 100 mg q8w 

Continue guselkumab 100 mg q8w 

Guselkumab 
100 mg at 
Weeks 16 
and 20, then q8w

Placebo

Adalimumab 80 mg at 
Week 0, 40 mg at Week 1, 
then q2w

Active-comparator Period

Placebo-
crossover

Placebo-
controlled

Open-label
Randomized Withdrawal 

and Retreatment

Weeks 40 16
PE
SE

24
SE

28 10076 252† 264‡
5 Year
DBL

The proportions of patients who achieved PASI 90, PASI 100, IGA 0/1, or IGA 0 were not impacted by the development 
of ADA to GUS

No direct association between the development of ADA and development of ISRs was apparent through  
Week 264. However, the small number of patients who were ADA positive and/or had ISRs limits drawing a definitive 
conclusion. 

Among the 13 patients who were positive for NAbs, all maintained IGA 0/1 and/or PASI 90 responses; 1 patient 
experienced a mild ISR after developing NAbs

Table 1. Proportions of Patients With Clinical Response at Week 252 by ADA Status Through 5 Years; GUS-treated Patientsa With 
Samples Evaluable for Immunogenicity

VOYAGE 1 VOYAGE 2

Negativeb Positivec Negativeb Positivec

Efficacy

Patients treated with GUSd 536 101 619 117

PASI 90 445 (83.0) 87 (86.1) 505 (81.7) 94 (80.3)

PASI 100 280 (52.2) 57 (56.4) 323 (52.3) 67 (57.3)

IGA 0/1e 437 (81.5) 89 (88.1) 527 (85.1) 95 (81.2)

IGA 0e 292 (54.5) 58 (57.4) 337 (54.4) 70 (59.8)

Data are presented as n (%). 
ADA, anti-drug antibodies; GUS, guselkumab; IGA , Investigator’s Global Assessment; IGA 0, cleared psoriasis; IGA 0/1, cleared or minimal psoriasis; PASI, Psoriasis Area  
and Severity Index; PASI 90, nearly complete clearance (≥90% improvement); PASI 100, complete clearance (100% improvement). 
aIncludes patients who received ≥1 dose of GUS, including those who crossed over from placebo or adalimumab. 
bIncludes all patients whose last sample was negative and excludes patients who were positive for antibodies to GUS through Week 264. 
cIncludes all patients who had ≥1 positive sample (treatment-boosted or treatment-induced) at any time after their first GUS administration through Week 264. 
dIncludes patients who had ≥1 evaluable sample after their first GUS administration and for whom efficacy assessments at Week 252 were performed. 
eIGA results were not available for 1 patient in VOYAGE 2. 

Table 2. Proportions of Patients With ISRs by ADA Status Through 5 Years; GUS-treated Patientsa With Samples Evaluable for 
Immunogenicity

VOYAGE 1 VOYAGE 2

Negativeb Positivec Negativeb Positivec

Safety

Patients treated with GUSd 659 111 797 146

Patients with ISRs 33 (5.0) 9 (8.1) 41 (5.1) 15 (10.3)

Number of GUS injections 17578 3158 20760 3832

Injections with ISRs 66 (0.4) 18 (0.6) 37 (0.2) 50 (1.3)

Data are presented as n (%). 
ADA, anti-drug antibodies; GUS, guselkumab; ISRs, injection site reactions. 
aIncludes patients who received ≥1 dose of GUS, including those who crossed over from placebo or adalimumab. 
bIncludes all patients whose last sample was negative and excludes patients who were positive for antibodies to GUS through Week 264. 
cIncludes patients who had ≥1 positive sample at any time after their first GUS administration through Week 264. 
dIncludes patients who had ≥1 evaluable sample after their first GUS administration.