klf

CID 5951923 is an inhibitor of KLF5 transcription factor with an IC50 of 603 nM.

SR15006 is Krüppel-like factor 5 (KLF5) inhibitor (IC50 = 41.6 nM).

APTO-253 (LOR-253) inhibits c-Myc expression, stabilizes G-quadruplex DNA, and induces cell cycle arrest and apoptosis in acute myeloid leukemia cells. APTO-253 mediates anticancer activity through the induction of the KLF4 tumor suppressor.

ML264 (CID-51003603) is a selective kruppel-like factor 5 (KLF5) inhibitor, which potently Inhibits growth of Colorectal Cancer.

LN-439A is a novel tetrahydro-β-carboline small molecule that acts as a potent catalytic inhibitor of the BAP1 deubiquitinase. It induces ubiquitination and degradation of the KLF5 transcription factor by binding to the catalytic pocket of BAP1. In basal-like breast cancer (BLBC) models, LN-439A significantly inhibits tumor cell proliferation and migration, induces G2/M phase arrest and apoptosis, and exhibits superior water solubility compared to existing BAP1 inhibitors. Furthermore, inhibition of BAP1 enzymatic activity by LN-439A also destabilizes its substrates, suggesting potential application value in inflammation-related diseases.

Pterosin B is a salt-inducible kinase 3 (Sik3) signaling inhibitor widely found in leaves and shoots of green plants.Pterosin B promotes the expression of G6pc, protects against Ang II-induced cardiomyocyte hypertrophy, and acts through the regulation of the expression level of NAD(P)H oxidase 2/4.

Sp1-IN-1 is a selective inhibitor of specificity protein 1 (Sp1) that suppresses the proliferation of Hela and MCF-7 cells. This compound is applicable in cervical and breast cancer research.

SR18662, an optimized compund based on ML264 that inhibits Krüppel-like factor 5 (KLF5) with IC50 of 4.4 nM, reduces the viability of multiple colorectal cancer cell lines and induces apoptosis.

CKLF1-C27, a C-terminal peptide of CKLF1, effectively binds to and activates the CCR4 receptor, triggering the ERK1/2 pathway. Competing with CKLF1 for the CCR4 receptor, it neutralizes CKLF1's cellular effects. Additionally, CKLF1-C27 significantly promotes the proliferation of HUVECs and holds promise for psoriasis research [1].

CKLF1-C27 TFA, a C-terminal peptide of CKLF1, binds to the CCR4 receptor and activates the ERK1/2 pathway. It can abrogate the effect of CKLF1 on cells by competing for the CCR4 receptor and shows significant effects on promoting proliferation in HUVECs. CKLF1-C27 TFA has the potential for psoriasis research [1].

CKLF1-C19, the C-terminal peptide of human chemokine-like factor 1 (CKLF1), interacts with CCR4 and inhibits chemotaxis induced by CKLF1 and CCL17. It also suppresses allergic lung inflammation by inhibiting chemotaxis mediated by CCR3 and CCR4 [1].

2-(4-methoxyphenyl)-2-oxoethyl 2-hydroxy-5-methylbenzoate is a pro-neurotropic drug used to enhance cognitive function by increasing the synthesis and release of acetylcholine in the brain as well as by inhibiting the breakdown of acetylcholine by acetylcholinesterase.

WX2-43 is a PRMT5-KLF4 inhibitor. Biotin-labeled WX2-43 binds to GST-PRMT5 with a dissociation constant Kd of 11.0 nM. It binds to the L400 to M500 amino acid region of PRMT5 protein, effectively blocking the interaction between KLF4 and PRMT5 and inhibiting KLF4 methylation modification. Functionally, WX2-43 downregulates p21 expression and upregulates Bax level, thereby suppressing the progression of triple-negative breast tumors. It can be applied to mechanism research of triple-negative breast cancer and colorectal cancer.

Obeticholic Acid (6-ECDCA, INT-747) is a high-affinity, semisynthetic, bile acid-derived FXR agonist with an EC50 of 99 nM and is able to upregulate IκB-α, KLF-2, and KLF-4 expression. Obeticholic Acid (6-ECDCA, INT-747) also shows potential for treating hepatic steatosis, inflammation, and fibrosis while increasing insulin sensitivity.