Phanes Therapeutics Announces Clinical Collaboration with Merck to Evaluate PT886 in Combination with KEYTRUDA® for Claudin 18.2-Positive Gastric and Gastroesophageal Junction Cancers

On October 16, Phanes Therapeutics, Inc. reached a clinical collaboration agreement with Merck to study Phanes' world-firstClaudin 18.2/CD47 Bispecific Antibody PT886With MerckPD-1 Inhibitor KEYTRUDA® (Pembrolizumab)In combination therapy for Claudin18.2-positive gastric cancer or gastroesophageal junction (GEJ) cancer patients.

PT886 was developed through Phanes' proprietary bispecific antibody technology platforms, PACbody™ and SPECpair™, and received Orphan Drug Designation from the FDA last year.

Phanes is currentlyInThe United States is conducting a multi-center Phase I clinical trial of PT886 to evaluate the safety, tolerability, pharmacokinetics, and preliminary efficacy of PT886 in patients with locally advanced or metastatic gastric cancer, gastroesophageal junction cancer, and pancreatic cancer. These patients have experienced disease progression after receiving available standard therapies, or the standard therapies have been proven ineffective, intolerable, or deemed inappropriate (NCT05482893).

Phanes' next phase of research is to explore the therapeutic potential of PT886 in combination regimens for gastric cancer, gastroesophageal junction cancer, and pancreatic cancer. The clinical collaboration with Merck will evaluate the use of PT886 in combination with KEYTRUDA® in patients with claudin 18.2-positive gastric or gastroesophageal junction cancer who are receiving or not receiving chemotherapy.

PT886 is a first-in-class bispecific antibody targeting claudin18.2 and CD47. Constructed using Phanes' proprietary bispecific antibody technology platforms, PACbody™ and SPECpair™, PT886 has been granted Orphan Drug Designation by the FDA for the treatment of pancreatic cancer. PT886 can directly kill tumor cells through macrophage phagocytosis (ADCP activity) and natural killer cell cytotoxicity (ADCC activity). By simultaneously targeting claudin 18.2 and CD47 expressed on the surface of tumor cells, PT886 broadens the scope of tumor killing.

In addition, PT886 is expected to induce the presentation of tumor neoantigens by guiding tumor cells into phagocytic antigen-presenting cells (APCs), and indirectly activate T cells to kill claudin 18.2-expressing tumor cells by recognizing tumor neoantigens, thereby stimulating the adaptive immune system.

The anti-CD47 arm of PT886, through differentiated design, exhibits minimal binding to human red blood cells while maintaining strong binding activity to CD47 on the surface of tumor cells, thus offering an improved benefit/risk profile compared to other CD47 molecules.