1. JAK/STAT Signaling Stem Cell/Wnt Cell Cycle/DNA Damage Apoptosis
  2. STAT CDK c-Myc Apoptosis
  3. STAT3-IN-53

STAT3-IN-53 (Compound L20) 是一种 STAT3 抑制剂,Kd 为 6.16 μM。STAT3-IN-53 可直接结合 STAT3 的 SH2 结构域,抑制 Y705 位点的磷酸化,且不影响总 STAT3 蛋白水平。STAT3-IN-53 可下调 cyclin-D1c-Myc 的转录与表达。STAT3-IN-53 可诱导细胞周期阻滞并促进细胞凋亡 (Apoptosis)。STAT3-IN-53 对结直肠癌具有抗癌活性。

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STAT3-IN-53

STAT3-IN-53 Chemical Structure

CAS No. : 3113051-34-3

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

STAT3-IN-53 (Compound L20) is a STAT3 inhibitor with a Kd value of 6.16 μM. STAT3-IN-53 binds directly to the SH2 domain of STAT3, inhibits phosphorylation at the Y705 site without affecting the total STAT3 protein level, and suppresses the IL-6/JAK/STAT3 pathway. STAT3-IN-53 downregulates the transcription and expression of cyclin-D1 and c-Myc. STAT3-IN-53 induces cell cycle arrest and promotes Apoptosis. STAT3-IN-53 exhibits anticancer activity against colorectal cancer[1].

IC50 & Target[1]

STAT3

6.16 μM (Kd)

体外研究
(In Vitro)

STAT3-IN-53 可直接与重组全长野生型 STAT3 蛋白结合,其 Kd 值为 6.16 μM[1]
STAT3-IN-53 可在 HEK-BLUE-IL6 细胞中强效抑制 IL-6/JAK/STAT3 信号通路,其 IC50 为 0.89 μM[1]
STAT3-IN-53 (96 h) 可强效抑制 HCT116、HT29、SW480、MC38 和 CT26 结直肠癌细胞系的增殖,其中对 HCT116 细胞的活性最强 (IC50 = 0.45 μM)[1]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay[1]

Cell Line: HCT116, HT29, SW480, MC38, CT26 colorectal cancer cell lines
Concentration: concentration gradient (for IC50 determination)
Incubation Time: 96 h
Result: Exhibited potent antiproliferative activity across all tested colorectal cancer cell lines, with IC50 values of 0.45 ± 0.05 μM (HCT116), 1.80 ± 0.10 μM (HT29), 9.34 ± 0.79 μM (SW480), 2.33 ± 0.48 μM (MC38), and 5.14 ± 0.84 μM (CT26).

Western Blot Analysis[1]

Cell Line: HCT116 cells
Concentration: 0.5, 2.5 μM
Incubation Time: 24 h
Result: Dose-dependently suppressed STAT3 phosphorylation at the Y705 residue without altering total STAT3 protein levels.
Did not inhibit phosphorylation of STAT6 or SRC.
Dose-dependently downregulated cyclin-D1 expression.
体内研究
(In Vivo)

STAT3-IN-53 (5-20 mg/kg;腹腔注射;每日一次;12 天) 可在 C57BL/6J 小鼠中对皮下 MC38 结肠腺癌的生长呈现剂量依赖性抑制[1]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (male, SPF grade, 18-20 g, subcutaneous implantation of MC38 colon adenocarcinoma tumor fragments)[1]
Dosage: 5 mg/kg; 20 mg/kg
Administration: i.p.; once daily; 12 days
Result: Achieved a tumor growth inhibition (TGI) rate of 53.6% at 5 mg/kg.
Achieved a tumor growth inhibition (TGI) rate of 59.8% at 20 mg/kg.
Suppressed STAT3 Y705 phosphorylation in tumor tissues at 20 mg/kg.
Downregulated Cyclin-D1 and c-Myc protein expression in tumor tissues at 20 mg/kg.
Caused no treatment-related adverse events or body weight loss exceeding 10% during the 12-day dosing period.
分子量

678.73

Formula

C33H33F3N8O3S

CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

纯度 & 产品资料
参考文献
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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STAT3-IN-53
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HY-181514
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