MHC Activator

FKBP12 PROTAC dTAG-7 (dTAG-7) is a FKBP12^F36V PROTAC degrader. FKBP12 PROTAC dTAG-7 binds FKBP12^F36V and CRBN to form a complex, mediating degradation via the ubiquitin-proteasome system. FKBP12 PROTAC dTAG-7 mediates the degradation of FKBP12^F36V-tagged nuclear and cytoplasmic proteins, including BRD4, HDAC1, EZH2, MYC, PLK1, KRAS^G12V, and antigen fusion proteins. FKBP12 PROTAC dTAG-7 enhances MHC class I antigen presentation. FKBP12 PROTAC dTAG-7 is applicable to leukemia-related research.

Adrixetinib (Q702) is an orally active triple inhibitor against CSF1R, Mer, and Axl, with K_d values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. Adrixetinib acts as a potent immune modulator that remodels the tumor microenvironment. Adrixetinib increases the abundance of M1 macrophages and CD8⁺ T cells, while decreasing the levels of M2 macrophages and myeloid-derived suppressor cells (MDSCs). Adrixetinib upregulates the expression of MHC class I and E-cadherin in tumor cells. Adrixetinib shows remarkable antitumor efficacy in syngeneic mouse tumor models. Adrixetinib is suitable for the research of breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma.

Adrixetinib (Q702) TFA is an orally active triple inhibitor against CSF1R, Mer, and Axl, with K_d values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. Adrixetinib TFA acts as a potent immune modulator that remodels the tumor microenvironment. Adrixetinib TFA increases the abundance of M1 macrophages and CD8⁺ T cells, while decreasing the levels of M2 macrophages and myeloid-derived suppressor cells (MDSCs). Adrixetinib TFA upregulates the expression of MHC class I and E-cadherin in tumor cells. Adrixetinib TFA shows remarkable antitumor efficacy in syngeneic mouse tumor models. Adrixetinib TFA is suitable for the research of breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma.

MEDI-5083 is an Fc fusion protein that targets CD40 and is a CD40 agonist. MEDI-5083 stimulates CD40 signaling via NF-κB activation. MEDI-5083 upregulates MHCII, CD80, and CD86 expression, induces pro-inflammatory cytokine secretion, and enhances IFN-γ secretion by memory CD8⁺ T cells. MEDI-5083 can be used for the research of melanoma, colon carcinoma, and advanced solid tumors^[1][2].

TP1L is a potent and selective T-cell protein tyrosine phosphatase (TC-PTP) PROTAC degrader, with a DC₅₀ value of 35.8 nM. TP1L elevates the phosphorylation level of TC-PTP substrates including pSTAT1 and pJAK1. TP1L selectively enhances IFN-γ signaling and increases MHC-I expression. TP1L activates TCR signaling through increases phosphorylation of LCK. TP1L enhances CAR-T cell mediated tumor killing efficacy through activation of the CAR-T cells. TP1L can be used for the study of cancer. (Pink: TC-PTP ligand: (HY-138964), Blue: E3 ligase CRBN Ligand (HY-A0003), Black: Linker: (HY-140002)).

CliMB-325 is an HSP90 inhibitor that can induce MHC-I (EC₅₀ = 498 nM) expression on the surface of CT26 murine colorectal cancer cells. CliMB-325 enhances T cell activation and exhibits lower toxicity. CliMB-325 can be used for the study of colorectal cancer.

SBP-5147 is an orally active ULK1/ULK2 inhibitor, with an IC₅₀ of 2 nM against ULK1 and an IC₅₀ of 53 nM against ULK2. SBP-5147 inhibits the phosphorylation of Beclin-1 and Vps34, reduces autophagy flux, downregulates the expression of ATG13 and ATG101, upregulates the expression of MHC-I, induces caspase-dependent apoptosis, and decreases the viability of non-small cell lung cancer cells. SBP-5147 is applicable to research related to non-small cell lung cancer^[1].