IFNAR Modulator

IFN-α Receptor Recognition Peptide 1 (IRRP1) is an amino acid synthetic peptide and also a regulator of IFN-α Receptor. IFN-α Receptor Recognition Peptide 1 binds to IFNAR2, enhances the binding capacity of IFN-α receptor, and slightly increases the IFN-α-induced growth inhibitory activity. IFN-α Receptor Recognition Peptide 1 inhibits IFN-α-induced STAT1 phosphorylation and STAT-DNA binding by blocking the activation of IFNAR by IFN-α. IFN-α Receptor Recognition Peptide 1 increases the occupancy of IFN-α on cell surface receptors, enhances the phosphorylation activation of ISGF3, and elevates IFN-α-induced antiviral activity. IFN-α Receptor Recognition Peptide 1 can be used in studies related to encephalomyocarditis virus infection.

IFN-α Receptor Recognition Peptide 1 acetate (IRRP1 acetate) is an amino acid synthetic peptide and also a regulator of IFN-α Receptor. IFN-α Receptor Recognition Peptide 1 acetate binds to IFNAR2, enhances the binding capacity of IFN-α receptor, and slightly increases the IFN-α-induced growth inhibitory activity. IFN-α Receptor Recognition Peptide 1 acetate inhibits IFN-α-induced STAT1 phosphorylation and STAT-DNA binding by blocking the activation of IFNAR by IFN-α. IFN-α Receptor Recognition Peptide 1 acetate increases the occupancy of IFN-α on cell surface receptors, enhances the phosphorylation activation of ISGF3, and elevates IFN-α-induced antiviral activity. IFN-α Receptor Recognition Peptide 1 acetate can be used in studies related to encephalomyocarditis virus infection.

PTPN2/1-IN-4 (Compound WS35) is an orally active, dual-functional inhibitor of PTPN1 and PTPN2 with IC₅₀s of 12.8 and 5.8 nM for PTPN1 and PTPN2, respectively. PTPN2/1-IN-4 modulates the IFNγ-JAK-STAT signaling pathway and significantly augments CD8+ T-cell tumor infiltration. PTPN2/1-IN-4 has potent anticancer activity, robustly inhibiting tumor growth both as a monotherapy and in combination with an anti-PD-1 antibody in B16-OVA syngeneic mouse models.

BI-1607 is a humanized monoclonal antibody targeting FcγRIIB/CD32b. BI-1607 selectively blocks inhibitory FcγRIIB signaling, abrogates its inhibitory function, redirects tumor cell-bound antibodies to activating FcγRs, and its modified Fc region prevents the binding of its own Fc segment to FcγRs. BI-1607 reduces αPD-1 trogocytosis, enhances the effector functions of anti-tumor antibodies (including ADCP and ADCC, promotes intratumoral regulatory T cell (Treg) depletion, myeloid cell reprogramming, induction of interferon-γ (IFN-γ) and CXCL10, and increases the number of activated effector CD8⁺ T cells. BI-1607 can be used in research related to colorectal cancer, HER2-positive advanced solid tumors, HER2-positive locally advanced or metastatic breast cancer, and HER2-positive metastatic gastric cancer.