2. Cell Cycle/DNA Damage Apoptosis Epigenetics
  3. CDK Apoptosis PARP Caspase Bcl-2 Family
  4. CDK9-IN-47

CDK9-IN-47 是一种口服有效且选择性 CDK9 抑制剂，IC50 为 1.4 nM。CDK9-IN-47 可抑制肿瘤细胞增殖、迁移和侵袭，诱导细胞凋亡 (apoptosis)。CDK9-IN-47 可用于三阴性乳腺癌的研究。

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CDK9-IN-47

CDK9-IN-47 Chemical Structure

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CDK9-IN-47 相关抗体

Top Publications Citing Use of Products

查看 CDK 亚型特异性产品:

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CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85 CDK10 CDK15 CDK17 CDK18 CDK20 PITSLRE

查看 PARP 亚型特异性产品:

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PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

查看 Caspase 亚型特异性产品:

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

查看 Bcl-2 Family 亚型特异性产品:

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

CDK9-IN-47 is an orally active and selective CDK9 inhibitor with an IC50 of 1.4 nM. CDK9-IN-47 inhibits tumor cell proliferation, migration and invasion, and induces apoptosis. CDK9-IN-47 can be used for the research of triple-negative breast cancer[1].

体外研究
(In Vitro)

CDK9-IN-47 (compound HS34) (72 h) 可强效抑制多种乳腺癌细胞系的增殖，且在处理 72 h 后对正常心肌细胞和肝细胞无细胞毒性 (GI50 > 10 μM)[1]。
CDK9-IN-47 (0.1-1.0 μM; 24 h) 以剂量依赖的方式消除 MDA-MB-231 和 4T1 三阴性乳腺癌 (TNBC) 细胞的克隆形成潜能[1]。
CDK9-IN-47 (0.1-3.0 μM; 8-24 h) 可在 MDA-MB-231 和 4T1 三阴性乳腺癌 (TNBC) 细胞中诱导剂量依赖性凋亡，抑制细胞的迁移与侵袭能力[1]。
CDK9-IN-47 (0.1-1.0 μM; 8 h) 可选择性抑制 MDA-MB-231 和 4T1 三阴性乳腺癌 (TNBC) 细胞中由 CDK9 驱动的转录过程，表现为 p-Ser2 CTD 水平降低、c-Myc 和 Mcl-1 表达下调，以及 cyclin T1 水平下降[1]。

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

CDK9-IN-47 相关抗体:

Cell Proliferation Assay[1]

Cell Line: Multiple breast cancer and normal cell lines (MDA-MB-231, MDA-MB-435, BT-549, 4T1, MCF-7, MCF-7-Pa, H9c2, THLE-2)
Concentration: /
Incubation Time: 72 h
Result: Exhibited a half-maximal growth inhibition (GI50) of 0.22 ± 0.09 μM in MDA-MB-231 TNBC cells.
Exhibited a GI50 of 0.68 ± 0.14 μM in MDA-MB-435 cells.
Exhibited a GI50 of 0.64 ± 0.09 μM in BT-549 TNBC cells.
Exhibited a GI50 of 0.53 ± 0.12 μM in 4T1 TNBC cells.
Exhibited a GI50 of 0.47 ± 0.17 μM in MCF-7 ER-positive breast cancer cells.
Exhibited a GI50 of 0.60 ± 0.21 μM in palbociclib-resistant MCF-7-Pa cells.
Showed minimal cytotoxicity in normal cell lines, with a GI50 > 10 μM in H9c2 cardiomyocytes and THLE-2 hepatocytes.

Western Blot Analysis[1]

Cell Line: MDA-MB-231 and 4T1 TNBC cells
Concentration: 0.3 μM, 1.0 μM, 3.0 μM
Incubation Time: 8 h
Result: Increased cleaved PARP and Caspase 3 levels.
Reduced levels of the antiapoptotic proteins XIAP and Bcl2.
药代动力学
(Parmacokinetics)
Species Dose Route Cmax Tmax T1/2 AUC0-t AUC0-∞ MRT0-t MRT0-∞ Bioavailability C0 CL Vd
Mice[1] 4 mg/kg i.v. / 0.083 h 2.53 h 1702.7 ng·h/mL 1767.3 ng·h/mL 1.63 h 1.88 h / 4723.9 ng/mL 2.14 L/h/kg 8.4 L/kg
Mice[1] 20 mg/kg p.o. 2176.0 ng/mL 1.0 h 5.44 h 3708.3 ng·h/mL 3763.0 ng·h/mL 3.36 h 3.87 h 43.6 % / / /
体内研究
(In Vivo)

CDK9-IN-47 (10-20 mg/kg；静脉注射；每日一次；连续 7 天) 在 BALB/c 小鼠 4T1 同源性三阴性乳腺癌模型中可产生性肿瘤生长抑制作用[1]。
CDK9-IN-47 (30-60 mg/kg；灌胃；间歇性给药；15 天) 可在 MDA-MB-231 人三阴性乳腺癌异种移植模型中产生显著的肿瘤生长抑制作用[1]。

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

Animal Model: BALB/c (syngeneic triple-negative breast cancer model via 4T1 cell implantation)[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: i.v.; daily; 7 days
Result: Achieved significant tumor growth inhibition, with reduced final tumor weights compared to vehicle control.
Achieved a tumor growth inhibition (TGI) of 56.1%, with a greater reduction in final tumor weights compared to the 10 mg/kg dose and the reference paclitaxel group.
Reduced expression of proliferation marker Ki-67, and CDK9 downstream proteins Mcl-1 and c-Myc.
Animal Model: Immunocompromised (xenograft triple-negative breast cancer model via MDA-MB-231 human cell implantation)[1]
Dosage: 30 mg/kg; 60 mg/kg
Administration: i.g.; intermittent schedule; 15 days
Result: Achieved significant tumor growth inhibition with reduced final tumor weights compared to vehicle control.
Achieved a tumor growth inhibition (TGI) of 71.3%, with a greater reduction in final tumor weights compared to the 30 mg/kg dose.
分子量

450.51

Formula

C25H27FN4O3
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

CDK9-IN-47 相关分类

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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.

Keywords:

CDK9-IN-47CDKApoptosisPARPCaspaseBcl-2 FamilyCyclin dependent kinasepoly ADP ribose polymeraseBcl2CDK9XIAPTwist1Snail1caspase 3MMP9triple-negative breast cancerInhibitorinhibitorinhibit

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