bcl-6

BCL6-IN-3 is a potent BCL6 inhibitor with GI50 of 70 nM in SU-DHL4 cells. BCL6-in-3 regulates cell activation, differentiation, DNA damage and apoptosis, and has antitumor activity.

BI-3812 is an inhibitor of BCL6. Which inhibiting the BTB domain of BCL6 (IC50: 3 nM). BI-3812 also has antitumor activity.

CID5721353 (BCL6 inhibitor) is a B-Cell Lymphoma 6 Inhibitor (BCL6 inhibitor) that disrupts BCL6/corepressor complexes in vitro and in vivo, and was shown to bind the critical site within the BTB groove.

FX1 is an effective and selective BCL6 inhibitor (IC50: 35 μM).

BCL6-IN-6 is an inhibitor of Bcl-6 and can be used in studies about diffuse large B-cell lymphoma. BCL6-IN-6 blocks the interaction of Bcl-6 with its corepressors and dose-dependently reactivates Bcl-6 target genes.

Bcl-2-IN-6 is a potent inhibitor of Bcl-2 (b-cell lymphoma-2) that downregulates Bcl-2 expression and increases the expression of p53, Bax, and caspase-7 mRNA. bcl-2-IN-7 induces cell cycle arrest and apoptosis in breast cancer MCF-7 cells. bcl-2-IN-7 acts on MCF-7 cells ( Bcl2-IN-7 showed good antitumor effects on MCF-7 cells (IC50: 20.91 μM), LoVo cells (IC50: 22.30 μM), HepG2 cells (IC50: 42.29 μM) and A549 cells (IC50: 48.00 μM).

Glycochenodeoxycholic Acid (Lithocholylglycine) is a glycine conjugate of lithocholic acid, a bile acid. It is increased in livers of mice that are fed diets supplemented with ursadeoxycholic acid. Glycolithocholic acid levels are decreased in lean mice treated with obestatin. Serum glycolithocholic acid levels increase with age in children.

TL4-12 is a specific MAP4K2/GCK inhibitor that inhibits IKZF1 and BCL-6.TL4-12 inhibits MM cell proliferation and induces apoptosis, and can be used in the study of multiple myeloma (MM).

BI-3802, a highly potent BCL6 degrader, targets and inhibits the Bric-à-brac (BTB) domain of BCL6, exhibiting an IC50 value of ≤3 nM. It induces polymerization of BCL6 and facilitates its degradation in a manner dependent on the E3 ligase SIAH1, demonstrating notable antitumor activity[1][2].

Glycochenodeoxycholic acid sodium salt is a bile salt formed in the liver from deoxycholic acid and glycine that induces apoptosis in hepatocytes. It acts as a detergent, dissolves fats for absorption, and is itself absorbed.

BCL6 PROTAC 1 is a selective B-cell lymphoma 6 (BCL6) proteolysis targeting chimera (PROTAC) that inhibits the BCL6 cell reporter with an IC50 of 8.8 µM and significantly degrades BCL6 in diffuse large B-cell lymphoma (DLBCL) cell lines, making it valuable for tumor-related research [1].

CCT374705, an orally active BCL6 inhibitor, exhibits potent antiproliferative effects in vitro and effectively inhibits tumor growth in a lymphoma xenograft mouse model [1].

BCL6-IN-7 (BCL6 inhibitor-7) is a BCL6 co-repressor interaction inhibitor with potential anticancer activity. It can be used for studying lymphomas.

ARV-393 HCl is an orally active and potent PROTAC targeting BCL6 with antitumor activity for the study of non-Hodgkin's lymphoma.

ARV-393 is a PROTAC degrader targeting BCL6 with the advantage of being highly potent and orally available.ARV-393 recruits BCL6 and E3 ligase cerebellum to rapidly degrade BCL6 through the cell's natural ubiquitin proteasome system for the treatment of diffuse large b-cell lymphoma (DLBCL) and non-Hodgkin's lymphoma (NHL).

BMS-986458 is a highly selective, orally active BCL6 PROTAC degrader. It specifically targets cereblon (CRBN) and the BCL6 N-terminal BTB domain to catalyze proximity-induced BCL6 degradation. BMS-986458 is applicable for research in B-cell non-Hodgkin lymphoma.

MNN-02-155 is a bivalent molecular glue that can simultaneously interact with both p300/CBP and BCL6. It effectively induces the activation of BCL6-targeted reporter genes and promotes cell death. This compound is used in the research of diffuse large B-cell lymphoma (DLBCL).

TCIP3 is a bivalent molecular glue (molecular glue) that can simultaneously bind to both p300/CBP and BCL6. It redirects p300 and CBP to activate programmed cell death genes, which are typically repressed by the oncogenic driver BCL6. TCIP3 is useful for studying diffuse large B-cell lymphoma (DLBCL) and is not toxic to untransformed tonsil lymphocytes or fibroblasts.

WK369 is an innovative small molecule inhibitor of BCL6, demonstrating remarkable bioactivity against ovarian cancer by inducing cell cycle arrest and triggering apoptosis. It binds directly to the BCL6-BTB domain, obstructing the interaction between BCL6 and SMRT, which results in the reactivation of p53, ATR, and CDKN1A.

JWZ-7-7-Neg1, a neighboring transcription chemical inducer (TCIP), serves as a negative control. It exhibits reduced binding capabilities to BRD4 or BCL6 compared to JWZ-7-7, resulting in lower cytotoxicity towards DLBCL cells.

SMRT peptide, one of the corepressor factors interacting with the BCL6 BTB domain, binds to the BTB domain of BCL6 to enhance its transcriptional repression function. Additionally, SMRT peptide is utilized for studying protein-protein interactions.

BCOR(498-514), biotinylated, is the smallest BCL6 binding domain with a KD of 1.32 µM. It can block BCL6-mediated transcriptional repression and induce cell death in lymphoma cells.

EB-TCIP (BAK-04-212) is a bivalent molecule composed of AP1867 and BI-3812. It facilitates the reversible formation of a ternary complex between FKBPF36V and BCL6BTB, thereby recruiting FKBP12F36V-tagged EWS/FLI1 to DNA sites bound by the transcriptional regulator BCL6, rapidly inducing expression of BCL6 target genes such as SOCS2 and CXCL11. EWS/FLI1 is a fusion transcription factor found in Ewing sarcoma. EB-TCIP is applicable for studying transcriptional dysregulation in cancer.

1-[2,4-Dihydroxy-6-methoxy-3-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-2-propen-1-one (Xanthohumol) , prenylchacone flavonoid, is a natural product with multi-biofunctions purified from Hops Humulus lupulus,is effective against HIV-1 and might serve as an interesting lead compound. It may represent a novel chemotherapeutic agent for HIV-1 infection.