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STAT is a family of cytoplasmic protein that regulates many aspects of growth, survival and differentiation in cells. The transcription factors of this family are activated by Janus kinase and dysregulation of this pathway is frequently observed in primary tumours and leads to increased angiogenesis, enhanced survival of tumours and immunosuppression. Gene knockout studies have provided evidence that STAT proteins are involved in the development and function of the immune system and play a role in maintaining immune tolerance and tumour surveillance. STAT proteins were originally described as latent cytoplasmic transcription factors that require phosphorylation for nuclear retention. The unphosphorylated STAT proteins shuttle between cytosol and the nucleus waiting for its activation signal. Once the activated transcription factor reaches the nucleus, it binds to consensus DNA-recognition motif called gamma-activated sites (GAS) in the promoter region of cytokine-inducible genes and activates transcription of these genes.

Cat. No. Product Name CAS No. Information



SH5-07 (SH-5-07, SH 5-07) is a potent, selective small-molecule STAT3 inhibitor with IC50 of 3.9 uM; preferentially inhibits Stat3:Stat3 DNA-binding activity, shows no inhibition of Stat1:Stat1 or Stat5:Stat5 activity; exerts pY705 Stat3 inhibition in human glioma, breast, and prostate cancer cells, blocks STAT3-dependent gene transcription along with Bcl-2, Bcl-xL, Mcl-1, cyclin D1, c-Myc, and survivin expression; decreases the proliferation and viability of glioma, breast, and prostate cancer cells and v-Src-transformed murine fibroblasts harboring constitutively active STAT3; effectively inhibits tumor growth in mouse xenograft models of glioma and breast cancer.


HJC0152 hydrochloride


A potent, orally bioavailable STAT3 signaling inhibitor that exhibits promising antitumor effects in vitro and in vivo via inactivating STAT3 and downstream miR-21/β-catenin axis; potently inhibits MCF-7, MDA-MB-231, AsPC1 and Panc-1a cell with IC50 of 0.91, 1.64, 1.9 and 1.08 uM, respectively; suppresses HNSCC cell proliferation, arrests the cell cycle at the G0-G1 phase, induces apoptosis and reduces cell invasion in both SCC25 and CAL27 cell lines; inhibits nuclear translocation of phosphorylated STAT3 at Tyr705 and decreases VHL/β-catenin signaling activity via regulation of miR-21; suppresses MDA-MB-231 xenograft tumor growth in vivo.




ML116 is a novel selective STAT3 inhibitor with IC50 of 4.2 uM, does not inhibit STAT1, STAT5, or NFkB signaling pathways (IC50>50 uM); inhibits transcription of the STAT3-regulated gene BCL3, sslectively induces loss of viability of breast cancer cell lines such as MDA-MB-468 cells.




CPA-7 is a platinum-containing compound that disrupts STAT3 signaling, inhibits cell growth and induces apoptosis in STAT3-activated cancer cells; selectively and significantly inhibits Stat3 activation and DNA-binding activity, induces regression of colon tumors in mouse model at 5mg/kg, with the abrogation of persistent Stat3 activity in tumors.




A orally bioavailable small-molecule STAT3 inhibitor; inhibits the proliferation of both ER-positive, and ER-negative (triple negative) breast cancer cells with IC50 values of 1.76 uM and 1.97 uM, respectively; inhibits cell cycle progression and promotes apoptosis both in vitro and in vivo.




Debio-0617B is a first-in-class, multi-kinase inhibitor that targets pSTAT3 and/or pSTAT5 in cancer cells through combined inhibition of JAK, SRC, ABL, and class III/V RTKs (Kd<100 nM); showes dose-dependent inhibition of pSTAT3 in STAT3-activated carcinoma cell lines (IC50=175 nM); also showes potent antiproliferative activity in a panel of cancer cell lines and in patient-derived tumor xenografts.




Ochromycinone is a small-molecule inhibitor of STAT3; inhibits Stat3 DNA binding activity, Stat3 dimerization, and Stat3-dependent luciferase activity (20-30 uM); reduces the survival of breast carcinoma cells with constitutive Stat3 signaling; inhibits cell viability and growth and induces apoptosis through caspases 3, 8 and 9 pathways in human sarcoma cell lines.




An orally bioavailable, small-molecule inhibitor of STAT3 with Kd of 504 nM; blocks Stat3-pTyr peptide interactions and Stat3 activation at 4-6.8 uM, and selectively inhibits growth, survival, migration, and invasion of Stat3-dependent tumor cells; suppresses the expression of c-Myc, Cyclin D1, Bcl-xL, Survivin, VEGF, and KLF8, blocks Stat3-NF-κB cross-talk, and enhances E-cadherin expression; inhibits growth of human breast and lung tumor xenografts.




FLLL-32 is a cell-permeable analog of curcumin that inhibits JAK2-mediated phosphorylation of STAT3 on Tyr705 in cancer cells (IC50=5 uM); induces apoptosis in pancreatic and breast cancer cell lines; also inhibit colony formation in soft agar and cell invasion and exhibits synergy with Doxorubicin against breast cancer cells; decreases STAT3 DNA binding activity and expression, and induces apoptosis in several cancer cell lines.




InS3-54A18 is an active analog of inS3-54 targeting the DBD of STAT3 with IC50 of 8.8 uM in STAT3-dependent luciferase reporter assay, with increased specificity and pharmacological properties; not only binds directly to the DBD and inhibits the DNA-binding activity of STAT3 both in vitro and in situ but also effectively inhibits the constitutive and IL-6-stimulated expression of STAT3 downstream target genes; InS3-54A18 is completely soluble in an oral formulation and effectively inhibits lung xenograft tumor growth and metastasis with little adverse effect on animals.

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