CLN-619 inhibited the shedding of MICA/B to effectively restore cytotoxic signaling pathways in immune cells. Potent antitumor activity of CLN-619 as a monotherapy was observed in several preclinical models. Activity of CLN-619 required a functional Fcγ1 domain, suggesting the requirement of simultaneous engagement of NKG2D and cluster of differentiation 16A (CD16A) on immune cells for optimal cytotoxicity. The preclinical data reported here support the assessment of CLN-619 in patients with cancer.
7 months ago
Journal
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FCGR3A (Fc Fragment Of IgG Receptor IIIa) • MICA (MHC Class I Polypeptide-Related Sequence A) • MICB (MHC Class I Polypeptide-Related Sequence B) • NKG2D (killer cell lectin like receptor K1)
Given the pan-cancer expression of MICA/MICB in both solid and hematological malignancies, CLN-619 is expected to have broad anti-tumor activity. CLN-619 is currently being investigated in a Phase 1 clinical trial for the treatment of patients with advanced solid tumors.
over 3 years ago
Clinical
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MICA (MHC Class I Polypeptide-Related Sequence A) • MICB (MHC Class I Polypeptide-Related Sequence B) • NKG2D (killer cell lectin like receptor K1)