MHC

AI-10-49 is a protein-protein interaction inhibitor that selectively binds to CBFβ-SMMHC and disrupts its binding to RUNX1 with a FRET IC50 of 0.26 uM,

ZLDI-8 is an inhibitor of the metalloproteinase enzyme ADAM-17, targeting the cleavage of Notch protein. This compound effectively reduces the expression of proteins associated with pro-survival pathways and epithelial-mesenchymal transition (EMT). Additionally, ZLDI-8 functions as a competitive and irreversible inhibitor of the tyrosine phosphatase Lyp, exhibiting an IC50 of 31.6 μM and a Ki of 26.22 μM. Notably, ZLDI-8 demonstrates potent growth inhibition of MHCC97-H cells with an IC50 of 5.32 μM, making it valuable for research into cellular signaling and cancer biology.

Tkip is a selective inhibitor of JAK2, targeting the JAK2 autophosphorylation site. It effectively inhibits JAK2 autophosphorylation and the phosphorylation of the IFN-γ receptor subunit IFNGR-1, thereby reducing the antiviral effects of IFN-γ and downregulating MHC Class I molecule expression. Tkip is a valuable tool for investigating the IFN-γ signaling pathway and its implications in various biological processes.

SBP-5147 is a potent inhibitor of ULK1 and ULK2, exhibiting an IC50 of 2 nM for ULK1 and 53 nM for ULK2. This compound effectively inhibits the phosphorylation of Beclin-1 and Vps34, reduces autophagic flux, and downregulates the expression of key autophagy-related proteins ATG13 and ATG101. Additionally, SBP-5147 enhances MHC-I expression, induces caspase-dependent apoptosis, and decreases the viability of non-small cell lung cancer cells. Its mechanism of action makes SBP-5147 a valuable tool for research in non-small cell lung cancer and autophagy modulation.

Z-Val-Val-Nle-diazomethylketone is a selective inhibitor of cathepsin S (CATS). This compound effectively reduces the IFNg-induced upregulation of MHCII molecules, specifically HLA-DR and Ii-p33/35, while promoting an increase in the Ii-p10 protein level. It is valuable for research into dermatological conditions such as psoriasis, atopic dermatitis, and actinic keratosis.

AS2677131 is a potent and orally active inhibitor of PIKfyve, targeting the PIKfyve-c-Rel signaling pathway. It effectively inhibits the production of pro-inflammatory cytokines, including IL-12p40, IL-6, and IL-1β, by selectively blocking the DNA-binding activity of c-Rel to their respective promoters. Additionally, AS2677131 reduces MHC class II expression on B cells. This compound is valuable for research in the fields of inflammation and immunology, particularly in studies related to arthritis.

Adrixetinib is a potent triple inhibitor targeting CSF1R, Mer, and Axl, with Kd values of 8.7 nM, 0.8 nM, and 0.3 nM respectively. This compound serves as an effective immune modulator by remodeling the tumor microenvironment, enhancing the presence of M1 macrophages and CD8⁺ T cells while reducing M2 macrophages and myeloid-derived suppressor cells (MDSCs). Additionally, Adrixetinib increases the expression of MHC class I and E-cadherin in tumor cells, demonstrating significant antitumor efficacy in syngeneic mouse models. It is relevant for research involving breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma.

TMLB-C16 is a selective B3GAT3 inhibitor with a dissociation constant (KD) of 3.962 μM. This compound effectively suppresses cell proliferation and migration while inducing cell cycle arrest and apoptosis in hepatocellular carcinoma cell lines MHCC-97H and HCCLM3, exhibiting IC50 values of 6.53 μM and 6.22 μM, respectively. In vivo studies demonstrate that TMLB-C16 inhibits tumor growth in MHCC-97H and HCCLM3 xenograft models without significant toxicity. TMLB-C16 is a valuable tool for research in hepatocellular carcinoma.

MY-1B is a covalent inhibitor of the RNA methyltransferase NSUN2 (IC50: 1.3 μM), stereoselectively targeting active-site cysteine residues (C271). It also covalently binds to PSME1, disrupting the proteasome regulatory complex and downregulating specific MHC-I subtype presentation.

GSK484 is a selective inhibitor of peptidylarginine deiminase 4 (PAD4), effectively blocking the enzyme's catalytic activity to inhibit protein citrullination and neutrophil extracellular trap (NET) formation. This compound demonstrates anti-inflammatory properties by reducing histone H3 production, modulating MHC-I expression, and inhibiting CD8+ T cell activation and proliferation. Research applications include studies on rheumatoid arthritis, sickle cell disease, myocardial ischemia-reperfusion injury, and colitis, as well as investigations into intestinal microbial homeostasis and ferroptosis-related dysbiosis.

WNT7A-IN-1 sodium is a selective inhibitor of WNT7A that disrupts the interaction between WNT7A and its receptor FZD5, leading to enhanced expression of MHC-I. This reagent is known to significantly increase levels of MHC-I and phosphorylated p65 while decreasing active β-catenin expression. Additionally, WNT7A-IN-1 sodium acts as a photosensitizer in the green spectral region, making it suitable for applications in photodynamic therapy and immunological studies.

MHC02181 is a potent inhibitor of Autotaxin (ATX), demonstrating an IC50 value of 9.41 μM. By inhibiting ATX, it plays a critical role in modulating lysophosphatidic acid (LPA) production, which is involved in various physiological and pathological processes. This reagent is valuable for research applications focused on cancer progression, fibrosis, and other ATX-mediated diseases.

MHC00188 is an allosteric inhibitor of Autotaxin (ATX) with an IC50 of 2.53 μM. This compound modulates ATX activity, which plays a critical role in the production of lysophosphatidic acid (LPA), a signaling lipid involved in various physiological processes. MHC00188 is useful for research into cancer biology, inflammation, and other conditions related to aberrant LPA signaling.

WNT7A-IN-1 is a WNT7A inhibitor that disrupts the interaction between WNT7A and its receptor FZD5, leading to the upregulation of MHC-I expression. This compound enhances the expression of MHC-I and phosphorylated p65 while decreasing the levels of active β-catenin. Additionally, WNT7A-IN-1 serves as a photosensitizer in the green spectral region, making it valuable for research in cancer immunotherapy and photodynamic therapy applications.

BI-5756 is a selective CETP inhibitor and cannabinoid receptor 1 (CB1) agonist. It promotes a significant increase in HDL-C levels while reducing LDL-C levels, thereby improving lipid profiles. Additionally, BI-5756 enhances the function of regulatory T cells and preserves T cell-mediated anti-tumor activity, exhibiting direct anti-proliferative effects on tumor cells. This compound also upregulates the expression of MHC I, MHC II, and CD80 on tumor cells and demonstrates protective effects in graft-versus-host disease. BI-5756 is applicable in research related to oncology, graft-versus-host disease, and metabolic disorders.

D-α-Methyl DOPA is an inhibitor of the binding of DQ8 peptide to MHC class II molecules. By occupying a pocket in the DQ8 peptide binding groove, D-α-Methyl DOPA disrupts the presentation of DQ8 peptides to CD4+ T cells. This inhibition may play a role in modulating the immune response, potentially slowing the development or progression of type 1 diabetes and celiac disease. This compound is valuable in immunological research focused on T cell activation and autoimmune disease mechanisms.

ERAP1 modulator-2 is a potent inhibitor of the enzyme ERAP1, exhibiting an IC50 value of less than 100 nM. This compound effectively modulates the activity of ERAP1, influencing peptide trimming and presentation in the context of antigen processing. It is valuable for research applications focused on immune regulation, inflammation, and the modulation of major histocompatibility complex (MHC) class I-mediated responses.

SA-15-P is a potent inhibitor of the LAG-3/MHCII and LAG-3/FGL1 protein-protein interactions, with IC50 values of 4.21 μM and 6.52 μM, respectively. By disrupting these interactions, SA-15-P serves as a valuable tool in immunotherapy research, providing insights into immune regulation and the potential enhancement of anti-tumor responses. Its application facilitates the exploration of therapeutic strategies targeting LAG-3 in various disease contexts.