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Human Papillomavirus (HPV)-associated head and neck cancers

Human Papillomavirus, or HPV, is estimated to cause about 5% of cancers worldwide, including approximately 99% of cervical cancers, up to 60% of HNSCC, 70% of vaginal cancers and 88% of anal cancers. While most infections with HPV are cleared from the body with no lasting consequences, in some cases, HPV DNA becomes integrated into chromosomal DNA. When host cells take up this DNA, they express the HPV E6 and E7 proteins. The expression of these proteins can lead to alterations in cell cycle control, which in turn predisposes these cells to become cancerous.

Our solution: HB-200

HB-200 alternates the administration of both HB-201 (LCMV) and HB-202 (PICV), collectively “HB-200,” attenuated viral vectors, which on their own are replicating-based therapeutics expressing a non-oncogenic, but highly antigenic, E7E6 fusion protein from HPV16. We have observed strong immunogenicity and robust antitumor activity in mouse models for LCMV alone as well as for the sequential administration of LCMV and PICV.

We presented positive preliminary Phase 2 data in patients with recurrent/metastatic HPV16+ head and neck cancers in the first line setting in May 2023 and additional patient data in October 2023 at the European Society for Medical Oncology (“ESMO”) Congress 2023. Data showed 42% objective response rate for 19 evaluable checkpoint inhibitor (“CPI”)-naïve patients. These data represent a doubling of the historical response rate (19 percent) reported for pembrolizumab alone.

Based on this safety, anti-tumor activity and T cell response data observed in the Phase 2 portion of the Phase 1/2 clinical trial ( Identifier: NCT04180215), we are preparing to start a randomized Phase 2/3 trial of HB-200 in combination with pembrolizumab in the 1st-line setting for patients with R/M HPV16+ head and neck cancers.

KRAS-mutated Cancers

KRAS is a gene that acts as an on/off switch for cell growth. When there is a mutation, or error, in the gene, cells can grow out of control. KRAS mutations are among the most common mutations that cause cancer. While KRAS-mutated, tumor-specific treatments exist, there remains an opportunity to target a broader range of KRAS-mutations simultaneously to potentially help more people impacted by these cancers.

KRAS mutations can be associated with poor prognosis and are common in many cancers, including pancreatic (≥60%), colorectal (30%-40%) and lung cancers (15%-20%).  Until recently, there has been no significant clinical success targeting KRAS in cancer; however, several therapies specifically targeting the KRAS G12C mutation have shown promising activity in lung cancer.  There is a need to improve upon the efficacy of current KRAS-targeted therapies while maintaining treatment tolerability and to expand KRAS-targeted therapy to other tumor types with high rates of KRAS mutations beyond lung cancer, including pancreatic and colorectal cancers.  Immunotherapeutic approaches and treatments that are able to target a broader range of KRAS mutations may help improve upon current KRAS-targeted therapy and provide new therapeutic options for patients with KRAS-mutated cancers.

Our solution: HB-700

HB-700 is an investigational arenaviral immunotherapy designed to treat KRAS-mutated lung, colorectal, pancreatic and other cancers. HB-700 is a replicating 2-vector therapy that targets the most common KRAS mutations: (G12D, G12V, G12R, G12C and G13D) and thereby benefits more patients than single mutation inhibitors.

HOOKIPA continues its Investigational New Drug (“IND”) application-enabling activities and we are on track to submit an IND in the second quarter of 2024.