Primary analysis of the registration-intended cohort of

patients with anti–PD-1–failed melanoma from the

IGNYTE trial of RP1 plus nivolumab, including clinical
subgroup and initial biomarker data
Michael K Wong1*, Praveen K Bommareddy2*, Mark R Middleton3, Mohammed M Milhem4, Joseph J Sacco5, Judith
Michels6, Gino K In7, Eva Muñoz Couselo8, Dirk Schadendorf9, Georgia M Beasley10, Jiaxin Niu11, Bartosz Chmielowski12,
Trisha M Wise-Draper13, Tawnya Lynn Bowles14, Katy K Tsai15, Céleste Lebbé16, Caroline Gaudy-Marqueste17, Adel
Samson18, Jason A Chesney19, Ari M VanderWalde20, Marcus Viana2, Chris Tucci2, Tim Liu2, Laxminarasimha
Donthireddy2, Alina Monteagudo2, Junhong Zhu2, Jeannie W Hou2, Caroline Robert21
1University of Texas MD Anderson Cancer Center, Houston, TX, USA; 2Replimune, Inc., Woburn, MA, USA; 3Churchill Hospital and University of Oxford, Oxford, UK; 4Holden Comprehensive Cancer Center,
University of Iowa, Iowa City, IA, USA; 5The Clatterbridge Cancer Centre, Wirral, UK and University of Liverpool, Liverpool, UK; 6Département de Médecine Oncologique, Gustave Roussy, Villejuif, France;
7University of Southern California Norris Comprehensive Cancer Center, Los Angeles, CA, USA; 8Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron Hospital Medical Oncology Department,

Barcelona, Spain; 9West German Cancer Center, University Hospital Essen, Essen, Germany; 10Duke Cancer Institute, Duke University, Durham, NC, USA; 11Banner MD Anderson Cancer Center, Gilbert, AZ,
USA; 12Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, CA, USA; 13University of Cincinnati Cancer Center, University of Cincinnati, Cincinnati, OH, USA;
14Intermountain Medical Center, Murray, UT, USA; 15Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA; 16Université Paris Cité, AP-HP

Dermato-Oncology and CIC, Cancer Institute APHP. Nord–Université Paris Cité, INSERM U976, Saint Louis Hospital, Paris, France; 17Aix-Marseille Université, APHM, Centre de Recherche en Cancérologie de
Marseille (CRCM), INSERM, U1068, CNRS, UMR7258, UM105, Hôpital Timone, CEPCM, Dermatology and Skin Cancer Department, Marseille, France; 18Leeds Institute of Medical Research at St. James’s,
University of Leeds, Leeds, UK; 19James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA; 20West Cancer Center and Research Institute, Germantown, TN, USA; 21Gustave Roussy
and Paris-Saclay University, Villejuif, France
*Both authors contributed equally.

2
Presenter disclosure
• Michael K Wong has participated on a Data Safety Monitoring Board
or Advisory Board for Bristol Myers Squibb, Castle Biosciences, EMD-
Serono, ExiCure, Merck, Pfizer, and Regeneron
• This study is sponsored by Replimune, Inc. (Woburn, MA, USA).
Nivolumab was supplied by Bristol Myers Squibb

3
 Background
• There are limited treatment options for patients with anti–PD-1–
progressed melanoma1,2
• Responses to targeted anti–BRAF + MEK for BRAF-mutant melanoma are
usually not durable3
• Single-agent anti–PD-1 after confirmed progressive disease on anti–PD-1
yields a 6%–7% response rate4,5
• Nivolumab + ipilimumab is a potential option,2 but toxicity is high2,6
• Nivolumab + anti–LAG-3 offers sub-optimal efficacy7
• TIL therapy gives response rates of ~30%,8 but nearly all patients have
grade 4 toxicity9,10

LAG-3, lymphocyte activation gene 3; PD-1, programmed cell death protein 1; TIL, tumor-infiltrating lymphocyte.
1. Mooradian MJ, et al. Oncology. 2019;33(4):141-8. 2. National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®). Melanoma: Cutaneous. Version 2. 2024. 3. Dixon-Douglas JR, et al. Curr Oncol Rep. 2022;24(8):1071-9. 4. Beaver JA, et al.
Lancet Oncol. 2018;19(2):229-39. 5. Ribas A, et al. Lancet Oncol. 2018;19(5):e219. 6. Pires da Silva I, et al. Lancet Oncol. 2021;22(6):836-47. 7. Ascierto PA, et al. J Clin Oncol. 2023;41(15)2724-35. 8. Chesney J, et al. J Immunother Cancer. 2022;10(12):e005755. 9. US Food and Drug
Administration. BLA clinical review and evaluation - AMTAGVI. BLA 125773. Updated February 6, 2024. Accessed May 31, 2024. https://www.fda.gov/media/176951/download. 10. Sarnaik AA, et al. J Clin Oncol. 2021;39(24):2656-66.

4
 Oncolytic immunotherapy is intended to activate a systemic
anti-tumor response1
Injected tumor Immune response
Attenuated potent clinical Oncolytic
isolate of HSV-1 modified immunotherapy Dendritic cell
to express a fusogenic T-cell
glycoprotein and Dysregulated host antiviral
immune-stimulating response allows robust
proteins virus replication and tumor
Tumor cell death and Enhanced T-cell priming
lysis release of tumor antigens and activation

Release Local T-cell infiltration and killing of

of virus progeny Inflammation distant, non-injected tumors
Infection of more Generating a strong
Altering of tumor and durable systemic
Intact host antiviral tumor cells microenvironment anti-tumor immune
response: Normal response
tissue remains
undamaged

Injected
tumor

Healthy Tumor tissue Distant

tissue tumors
HSV-1, herpes simplex virus type 1.
1. Bommareddy PK, et al. Am J Clin Dermatol. 2017;18(1):1-15.

5
 Study design
28 days First dose 2 weeks RP1 + nivolumab 2 weeks 2 weeks
Nivolumab Nivolumab
Screening RP1 1×106 1×107 pfu/mL,
240 mg 480 mg (Q4W)
pfu/mL 240 mg
100-day
Anti–PD-1–failed
safety
cutaneous melanoma
Cycle 1 Cycles 2–8 Cycle 9 Cycles 10–30a follow-
(140 patients)
up

3-year follow-up from last patient enrolled

Tumor response assessment: Radiographic imaging at baseline and every 8 weeks from first dose and every 12 weeks after confirmation of response

Primary objective Key eligibility

• Safety and efficacy using mRECIST* v1.1 by independent central review Anti–PD-1–failed advanced melanoma; measurable disease; adequate organ function; no
(sensitivity analysis by RECIST v1.1) prior oncolytic therapy; ECOG performance status 0–1

Secondary objectives Criteria for prior anti–PD-1–failure

• ORR by investigator assessment (mRECIST* v1.1) Confirmed progression while being treated with at least 8 weeks of anti–PD-1 therapy,
• DOR, CR rate, DCR, and PFS by central and investigator assessment, alone or in combination; anti–PD-1 must be the last prior therapy. Patients on prior
1-year and 2-year OS adjuvant therapy must have confirmed progression while being treated with adjuvant
treatment (PD can be confirmed by biopsy)
* For mRECIST, PD must be confirmed by further progression at least 4 weeks after
initial PD; intended to better allow for pseudoprogression than RECIST v1.1
Primary analysis conducted when all patients had ≥12 months follow-up

aRP1 can be reinitiated beyond 8 cycles if protocol-specified criteria are met.

CR, complete response; DCR, disease control rate; DOR, duration of response; ECOG, Eastern Cooperative Oncology Group; mRECIST, modified RECIST; ORR, objective response rate; OS, overall survival; PD, progressive disease; PD-1, programmed cell death protein 1; PFS, progression-
free survival; pfu, plaque-forming unit; Q4W, every 4 weeks; RECIST, Response Evaluation Criteria in Solid Tumors.

6
 RP1 administration Injection administration
for superficial tumors For nonulcerated superficial tumor

• RP1 is injected into superficial and/or

Top-down view of skin

deep/visceral tumors
• Both superficial and deep/visceral tumors For ulcerated superficial tumor
may be injected in the same injection day
Inject around
• Deep/visceral injections are done by
the ulcer
ultrasound or CT
• The volume of RP1 is dependent on the
lesion size
Injection administration for
• Multiple tumors may be injected with up to
deep tumors
10 mL of RP1
• Generally, injections should be made from Radial injection or
largest to smallest lesions coaxial injection may be
used via image
guidance with
ultrasound or CT
CT, computed tomography.

7
Baseline clinical characteristics
• A “real world” anti–PD-1–failed melanoma population was enrolled
Patients, n (%) N = 140 Patients, n (%) N = 140
Age, median (range), y 62 (21–91) Prior therapy
Sex Anti–PD-1
Female 45 (32.1) Anti–PD-1 only as adjuvant therapy 36 (25.7)
Male 95 (67.9) Anti–PD-1 other than as adjuvant therapy 104 (74.3)
Stage Anti–CTLA-4
IIIb/IIIc/IVM1a 72 (51.4)
Anti–PD-1 combined with anti–CTLA-4 61 (43.6)
IVM1b/c/d 68 (48.6)
Anti–PD-1 treated with anti–CTLA-4 sequentially 4 (2.9)
BRAF status
Received BRAF/MEK therapy 17 (12.1)
Wild-type 87 (62.1)
Anti–PD-1 resistance category
Mutant 53 (37.9)
Primary resistancea 92 (65.7)
LDH level
Secondary resistanceb,c 48 (34.3)
LDH ≤ULN 92 (65.7)
LDH >ULN 47 (33.6) Due to the requirement that patients must have confirmed PD on an immediate
prior anti–PD-1–based therapy, most patients had 1 or 2 prior lines of therapy
Unknown 1 (0.7)
Baseline PD-L1 tumor expression The median (range) follow-up at the time of the primary analysis was
15.4 months (0.5–47.6 months)
Positive (≥1%) 44 (31.4) aPrimary resistance: Progressed within 6 months of starting the immediate prior course of anti–PD-1 therapy. bSecondary

Negative (<1%) 79 (56.4) resistance: Progressed after 6 months of treatment on the immediate prior course of anti–PD-1 therapy. cIncludes 1
patient with unknown resistance status.
Undetermined or missing 17 (12.1) CTLA-4, cytotoxic T-lymphocyte antigen 4; LDH, lactate dehydrogenase; PD, progressive disease; PD-1, programmed cell
death protein 1; PD-L1, programmed death-ligand 1; ULN, upper limit of normal.

8
 Primary efficacy analysis
By blinded, independent central review

Primary endpoint Sensitivity analysis

mRECIST v1.1 RECIST v1.1
(N = 140) (N = 140)
Confirmed best response, n (%)
CR 21 (15.0) 21 (15.0)
PR 26 (18.6) 25 (17.9)
SD 41 (29.3) 31 (22.1)
PD 43 (30.7) 54 (38.6)
ORR (confirmed CR+PR), n (%) 47 (33.6) 46 (32.9)
95% CI (25.8, 42.0) (25.2, 41.3)

• 1 in 3 patients (33.6%) experienced a confirmed objective response, 15.0% CR

CI, confidence interval; CR, complete response; mRECIST, modified RECIST; ORR, objective response rate; PD, progressive disease; PR, partial response; RECIST, Response Evaluation Criteria in Solid Tumors; SD, stable disease.

9
Duration of response

• Median (range) duration of response was 21.6 months (1.2+ to 43.5+ months)

10
 Efficacy
• Centrally reviewed mRECIST v1.1 responses (per protocol); all patients have ≥12 months follow-up

Single-agent Anti–PD-1/ Stage Stage Primary Secondary Anti–PD-1 Anti–PD-1

BOR All patients
anti–PD-1 CTLA-4 IIIb–IVa IVb–IVd resistance resistance adjuvant not adjuvant
n (%) (N = 140)
(n = 75) (n = 65) (n = 72) (n = 68) (n = 92) (n = 48a) (n = 36) (n = 104)

CR 21 (15.0) 16 (21.3) 5 (7.7) 17 (23.6) 4 (5.9) 16 (17.4) 5 (10.4) 11 (30.6) 10 (9.6)

PR 26 (18.6) 13 (17.3) 13 (20.0) 12 (16.7) 14 (20.6) 17 (18.5) 9 (18.8) 5 (13.9) 21 (20.2)

SD 41 (29.3) 20 (26.7) 21 (32.3) 24 (33.3) 17 (25.0) 22 (23.9) 19 (39.6) 10 (27.8) 31 (29.8)

PD 43 (30.7) 24 (32.0) 19 (29.2) 18 (25.0) 25 (36.8) 31 (33.7) 12 (25.0) 9 (25.0) 34 (32.7)

ORR 47 (33.6) 29 (38.7) 18 (27.7) 29 (40.3) 18 (26.5) 33 (35.9) 14 (29.2) 16 (44.4) 31 (29.8)

• Consistent response rates were seen across patient subgroups, including the following:
• 27.7% ORR in patients who had prior anti–PD-1 and anti–CTLA-4
• 35.9% ORR in patients who had primary resistance to anti–PD-1
aIncludes 1 patient with unknown resistance status.
BOR, best overall response; CR, complete response; CTLA-4, cytotoxic T-lymphocyte antigen 4; mRECIST, modified Response Evaluation Criteria in Solid Tumors; ORR, objective response rate; PD, progressive disease; PD-1, programmed cell death protein 1; PR, partial response;
SD, stable disease.

11
 Change in size of individual injected and non-injected lesions
for responding patients (superficial and deep/visceral)
Number (%) of measured
lesions for responders
(CR or PR; N = 47)
Injected Non-injected
(n = 79) (n = 123)
Number of lesions with:
No reduction 1 (1.3) 4 (3.3)
Any reduction 78 (98.7) 119 (96.7)
Best reduction >0% to <30% 4 (5.1) 21 (17.1)
Best reduction ≥30% to 31 (39.2) 48 (39.0)
<100%
Best reduction of 100% 43 (54.4) 50 (40.7)

• Injected and non-injected lesions responded with similar frequency, depth, duration, and kinetics
• Most lesions (85%) had a reduction ≥30%
All measurable lesions (10 max if >10 were present) measured by central review for each patient with a best response of confirmed CR or PR (excludes new lesions). Central reviewers were blinded to lesion injection status.
CR, complete response; PR, partial response.

12
Responses in injected and non-injected lesions
Responses observed, including visceral non-injected lesions

Patient example 1 Patient example 2 • Tumor reduction seen in

53 out of 60 non-injected
visceral organ lesions
Best percentage change from baseline

20
• Injected and non-injected
0
lesions responded with
–20 similar frequency, depth,
–30 and duration
–40
• Responses were not
–60 driven by injected lesions
alone
–80

–100

Patients
Injected Non-injected

13
Anti-tumor effect of non-injected lesions in visceral organs of
responding patients (N = 47)
Location of
n* (lesions) Any Reduction >0 to <30% ≥30% to <100% 100%
visceral lesions
Lung 29 28 (96.6%) 7 (24.1%) 9 (31%) 12 (41.4%)
Liver 15 15 (100%) 4 (26.7%) 5 (33.3%) 6 (40%)
Adrenal 3 1 (33.3%) 0 0 1 (33.3%)
Ovary 1 1 (100%) 0 0 1 (100%)
Spleen 6 5 (83.3%) 5 (83.3%) 0 0
Pleura 2 2 (100%) 0 1 (50%) 1 (50%)
Brain 3 1 (33.3%) 1 (33.3%) 0 0
Pancreas 1 0 0 0 0
Total 60 53 (88.3%) 17 (28.3%) 15 (25%) 21 (35%)

• RP1 + nivolumab induced deep responses in non-injected lesions in visceral organs, including those distant
from the injection site
*Includes 6 new lesions that appeared while on study

14
 Patient example: Prior atezolizumab + cobimetinib, ipilimumab, SX-682
(CXCR inhibitor) + atezolizumab, ipilimumab + nivolumab
Baseline
15 months

• Responses in non-injected distant and visceral tumors, including healing response

in lytic bone lesions (new marginal sclerosis and internal bone formation) Injected Non-injected
Based on measured lesions by Independent Central Review assessment.

15
 Progression-free survival and overall survival
Progression-free survival Overall survival
1 1

0.9 0.9
75.3%
0.8 0.8
63.3%
Probability of PFS

0.7 0.7

Probability of OS
54.8%
0.6 0.6

0.5 0.5
0.4 32.8% 0.4

0.3 0.3

0.2 0.2

0.1 0.1
Censored Censored
0 0

0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48
Time (months) Time (months)
Number of patients at risk: Number of patients at risk:

140 83 52 46 39 32 23 21 16 14 10 7 3 2 2 1 140 127 116 104 95 72 63 52 43 35 29 17 9 6 5 3 0

• Twelve-month PFS was 32.8%; median PFS was 3.7 months (95% CI, 3.4–5.0)
• One-, 2-, and 3-year OS rates were 75.3%, 63.3%, and 54.8%, respectively; median OS has not been reached

CI, confidence interval; PFS, progression-free survival; OS, overall survival.

16
 Safety profile: Treatment-related AEs (N = 141)
Related to either RP1 or nivolumab
TRAEs occurring in ≥5% of patients RP1 combined with nivolumab is generally well
Preferred term, n (%) (N = 141)
tolerated
All Grades Grade 3–4
≥1 TRAE 126 (89.4) 18 (12.8) • Predominantly grade 1 and 2 constitutional-
Fatigue 46 (32.6) 1 (0.7) type side effects
Chills 45 (31.9) 0 (0.0)
Pyrexia 43 (30.5) 0 (0.0) • Low incidence of grade 3 events (none occurring
Nausea 31 (22.0) 0 (0.0) in >5% of patients); five grade 4 events in total
Influenza-like illness 25 (17.7) 0 (0.0)
Injection-site pain 21 (14.9) 0 (0.0) • No grade 5 events
Diarrhea 20 (14.2) 1 (0.7)
Vomiting 19 (13.5) 0 (0.0) Additional grade 3/4 TRAEs (grade 4 TRAEs are italicized):
Headache 18 (12.8) 0 (0.0) • Two events each (1.4%): Hypophysitis and rash maculo-papular
Pruritus 18 (12.8) 0 (0.0) • One event each (0.7%): Abdominal pain, acute left ventricular failure, amylase
Asthenia 14 (9.9) 1 (0.7) increased, cancer pain, cytokine release syndrome, eczema, enterocolitis, extranodal
Arthralgia 10 (7.1) 1 (0.7) marginal zone B-cell lymphoma (MALT type), hepatic cytolysis, hyponatremia,
Decreased appetite 9 (6.4) 1 (0.7) immune-mediated enterocolitis, infusion-related reaction, left ventricular
Myalgia 9 (6.4) 0 (0.0) dysfunction, lipase increased, memory impairment, meningitis aseptic, muscular
Cough 8 (5.7) 0 (0.0) weakness, myocarditis, palmar-plantar erythrodysesthesia syndrome, paresthesia,
Rash 8 (5.7) 0 (0.0) peripheral sensory neuropathy, radiculitis brachial, sinus arrhythmia, splenic rupture,
Injection-site reaction 7 (5.0) 0 (0.0) tricuspid valve incompetence, tumor pain, type 1 diabetes mellitus
Vitiligo 7 (5.0) 0 (0.0)

AE, adverse event; MALT, mucosa-associated lymphoid tissue; TRAE, treatment-related AE.

17
 RP1 + nivolumab increased T-cell infiltration and PD-L1
expression
Reversal of T-cell deficiency Increase of T-cell infiltration

CD8+ T cell PD-L1 CD8+ T cell PD-L1

Screening

Screening
Day 43

Day 43
101-1122-2048 101-3314-2013

PD-L1, programmed death-ligand 1.

18
 Increase in CD8+ T-cell infiltration and PD-L1 expression
CD8+ T-cell score PD-L1 expression (CPS)
40 100 Screening (n = 68) Cycle 4 (n = 68)
CD8+ INTR:
0 90
35 34
1+
80
30 2+
30
27 70
3+
Number of patients

25 60

CPS%
20 50
20 19
40
15
13
11 30
10
20

5 10
2
0
0
Screening Cycle 4 Screening Cycle 4
Visit Visit

• Available tumor biopsies showed increased CD8+ T-cells score 37/78 (47%) and PD-L1 expression 39/68
(57%) at day 43 compared with baseline, demonstrating immune activation
CPS, combined positive score; PD-L1, programmed death-ligand 1.

19
 Gene expression changes associated with immune activation*
Changes in genes from screening to day 43

CD8+ Cytotoxic cells DC Macrophage

NR = Non-responder
R = Responder

Down from SCR <--Log2 fold change ---> Up from SCR

Day 43 Day 43 Day 43 Day 43

Exhausted Infla cytokines NK CD56 dim TH1 cells TIGIT TIS

Day 43 Day 43 Day 43 Day 43 Day 43 Day 43

*Data from previous IGNYTE cohorts.

DC, dendritic cell; Infla, inflammatory; NK, natural killer cell; NR, non-responder; R, responder; SCR, screening; TH, T helper; TIGIT, T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains; TIS, tumor inflammation signature.

20
 Conclusions
• Efficacy
• RP1 combined with nivolumab after confirmed progression on anti–PD-1 therapy alone or combined with anti–CTLA-4 demonstrated a
clinically meaningful rate and duration of response
• ORR 33.6%; median DOR of 21.6 months
• Responses occur in patients with advanced disease, including in non-injected visceral lesions
• Clinically meaningful activity across all subgroups, including after combined anti–PD-1/CTLA-4 and in primary anti–PD-1 resistant disease
• Survival
• While median OS has not yet been reached, 1- (75.3%), 2- (63.3%), and 3-year (54.8%) survival rates are promising and further
demonstrate durable clinical benefit
• Safety
• The safety profile was favorable, with generally transient grade 1–2 side effects
• Biomarkers
• Initial biomarker data demonstrate increased CD8+ T-cell infiltration, PD-L1 expression, and interferon gene expression signature changes
associated with the induction of an inflamed tumor phenotype
• Next steps
• The IGNYTE-3 confirmatory phase 3 trial evaluating RP1 + nivolumab vs physician’s choice in melanoma that has progressed on anti–PD-1
and anti–CTLA-4 is currently recruiting (NCT06264180)

CTLA-4, cytotoxic T-lymphocyte antigen 4; DOR, duration of response; ORR, objective response rate; OS, overall survival; PD-1, programmed cell death protein 1; PD-L1, programmed death-ligand 1.

21
 Acknowledgements
• We would like to thank the patients for their participation in the trial, as well as their family members
• We would also like to thank the site staff and principal investigators for their critical contributions to this study

Dr. Jason A Chesney University of Louisville Dr. Georgia M Beasley Duke Cancer Institute Dr. Judith Michels Institut Gustave Roussy
Dr. Jiaxin Niu Banner MD Anderson Cancer Center Dr. Trisha M Wise-Draper University of Cincinnati Cancer Center Dr. Ana María Arance
Hospital Clinic Barcelona
Fernandez
Intermountain Cancer Center - Saint Dr. Robert McWilliams Mayo Clinic - Minnesota
Dr. Terence Rhodes Dr. Eva Muñoz Couselo Hospital Universitari Vall d'Hebron
George
Dr. Mahesh Seetharam Mayo Clinic - Arizona
UCSF/Helen Diller Family Hospital Universitario Virgen de la
Dr. Katy K Tsai Dr. Pablo Cerezuela
Comprehensive Cancer Center Dr. Issam Makhoul CARTI Cancer Center Arrixaca
West Cancer Clinic and Research Dr. Michael K Wong MD Anderson Cancer Center Dr. Miguel Sanmamed Clinica Universitaria de Navarra
Dr. Ari M VanderWalde
Institute
Dr. Céleste Lebbé Hôpital Saint Louis APHP Dr. Maria Luisa Limon Hospital Universitario Virgen del Rocio
University of Washington
Dr. Evan Hall
Seattle Cancer Care Alliance Dr. Sophie Dr. Mark Middleton Oxford University Hospital
CHU Dijon-Bourgogne
Dr. Tawnya Lynn Bowles Intermountain Medical Center Dalac-Rat
Dr. Kevin Harrington Royal Marsden Hospital
Dr. Mohammed M Dr. Caroline Gaudy- CHU de La Timone Aix-Marseille
University of Iowa Marqueste University Dr. Joseph J Sacco Clatterbridge Cancer Centre
Milhem
Dr. Gregory Daniels Moores UCSD Cancer Center Dr. Charlée Nardin CHU Besancon – Hôpital Jean Minjoz Dr. Adel Samson University of Leeds
Dr. Antoine Italiano Institut Bergonié The Beatson West of Scotland Cancer
Dr. Bartosz Chmielowski University of California, Los Angeles Dr. Patricia Roxburgh
Center
Dr. John Fruehauf University of California, Irvine Dr. Mona Amini-Adle Centre Léon Bérard
Dr. Dirk Schadendorf University Hospital Essen
USC Norris Comprehensive Cancer
Dr. Gino K In
Center

The IGNYTE study is currently recruiting patients with anti–PD-1–failed NMSC and anti–
Additional information can be obtained by
PD-1–failed MSI-H/dMMR solid tumors. To learn more about enrolling your patient,
visiting Clinicaltrials.gov (NCT03767348).
contact [email protected] or +1 (781) 222 9570.

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