• General Dermatology
  • Eczema
  • Alopecia
  • Aesthetics
  • Vitiligo
  • COVID-19
  • Actinic Keratosis
  • Precision Medicine and Biologics
  • Rare Disease
  • Wound Care
  • Rosacea
  • Psoriasis
  • Psoriatic Arthritis
  • Atopic Dermatitis
  • Melasma
  • NP and PA
  • Skin Cancer
  • Hidradenitis Suppurativa
  • Drug Watch
  • Pigmentary Disorders
  • Acne
  • Pediatric Dermatology
  • Practice Management

Replimune and Incyte to Collaborate on Clinical Trial to Study RP1 in Combination With INCB99280 for CSCC

Press Release
Dermatology TimesDermatology Times, September 2023 (Vol. 44. No. 09)
Volume 44
Issue 09

Both companies are hoping to make a positive impact in the neoadjuvant setting of cutaneous squamous cell carcinoma.


Replimune Group and Incyte recently announced their joint clinical trial collaboration and supply agreement to study Replimune’s RP1 in combination with Incyte’s INCB99280 for the treatment of cutaneous squamous cell carcinoma (CSCC). From their agreement, Incyte will initiate and sponsor the clinical trial of INCB99280 and RP1 in patients with high-risk, resectable CSCC, with the clinical trial expected to begin in early 2024. Replimune will supply Incyte with RP1 for the study and share equally in the costs of the study.1

RP1 is Replimune’s lead oncolytic immunotherapy product candidate and is based on a proprietary new strain of herpes simplex virus engineered for robust tumor-selective replication and genetically armed with a fusogenic protein (GALV-GP R-) and GM-CSF, intended to maximize tumor killing potency, the immunogenicity of tumor cell death, and the activation of a systemic anti-tumor immune response.

Incyte’s INCB99280 is a potent and selective small molecule oral PD-L1 inhibitor, which has demonstrated promising clinical activity and safety in patients with solid tumors. INCB99280 is being evaluated in multiple phase 2 studies as monotherapy and in combination with other antitumor agents.

Replimune’s proprietary RPx platform is based on a potent HSV-1 backbone with payloads added to maximize immunogenic cell death and the induction of a systemic anti-tumor immune response. The RPx platform has a unique dual local and systemic mechanism of action (MOA) consisting of direct selective virus-mediated killing of the tumor resulting in the release of tumor derived antigens and altering of the tumor microenvironment to ignite a durable systemic response. According to Replimune, this MOA is expected to be synergistic with most established and experimental cancer treatment modalities, and, with a proven safety profile the RPx platform has the versatility to be developed alone or combined with a variety of other therapies.

Regarding their work together, Robert Coffin, the chief research and development officer of Replimune, said, “We are excited to enter into this collaboration with Incyte to explore the use of RP1 prior to surgery as we believe that our tumor-directed oncolytic immunotherapies could have a great impact in the neoadjuvant setting both in cutaneous squamous cell carcinoma and in other cancer types, given the high rates of complete responses we’ve seen to date, and data indicating RP1 is generally very well tolerated.”

“We look forward to collaborating with Replimune on this study evaluating INCB99280 and RP1 in patients with CSCC. Our oral PD-L1 program has shown promising safety and efficacy in early studies thus far, and we look forward to adding to the growing body of evidence for INCB99280 and learning more about its potential to improve clinical outcomes,” said Lance Leopold, MD, the group vice president of clinical development of hematology and oncology at Incyte.


1. Replmune and Incyte enter into clinical trial collaboration and supply agreement to evaluate RP1 and INCB99280 in patients with cutaneous squamous cell carcinoma. Incyte. July 31, 2023. Accessed July 31, 2023. https://investor.incyte.com/news-releases/news-release-details/replimune-and-incyte-enter-clinical-trial-collaboration-and

Related Videos
© 2024 MJH Life Sciences

All rights reserved.