2. Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR Cell Cycle/DNA Damage Epigenetics Apoptosis
  3. Anaplastic lymphoma kinase (ALK) mTOR PARP Caspase
  4. ALK-IN-26

ALK-IN-26 (compound 4a) 是 ALK 抑制剂，对 ALK 酪氨酸激酶的 IC50 值为7.0 μM。ALK-IN-26 有良好的药代动力学特性和血脑屏障通透性。ALK-IN-26 能够引起细胞凋亡、自噬和坏死。ALK-IN-26 能够用于胶质母细胞瘤研究。

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ALK-IN-26 Chemical Structure

ALK-IN-26 Chemical Structure

CAS No. : 2447607-85-2

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ALK-IN-26 相关抗体

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mTOR mTORC1 mTORC2

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

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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

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

ALK-IN-26 is an ALK inhibitor with IC50 value of 7.0 μM for ALK tyrosine kinase. ALK-IN-26 has good pharmacokinetic properties and blood-brain barrier (BBB) permeability. ALK-IN-26 can induce apoptosis, autophagy and necrosis. ALK-IN-26 can be used in glioblastoma studies[1].

体外研究
(In Vitro)

ALK-IN-26 (0.5-2 μM, 24 h) 在 GL216 细胞中能够抑制 ALK 的活性[1]。
ALK-IN-26 (0.5-10 μM, 24-72 h) 在 GL216、U87MG、Hela 细胞中能够抑制 GL216、U87MG 的活性，对 Hela 细胞活性的抑制有限[1]。
ALK-IN-26 (0.5-2 μM, 24 h) 在 GL216 细胞中能够降低 mTOR 蛋白水平的表达[1]。
ALK-IN-26 (0.5-2 μM, 24 h) 在 GL261 和 U87MG 细胞中显著降低 p-ERK1/2 蛋白水平、增强 p-JNK水平，对 p-AKT 和 p-STAT3 蛋白水平几乎不影响[1]。
ALK-IN-26 (0.5-2 μM, 24 h) 在 GL261 细胞中能够诱导细胞自噬[1]。
ALK-IN-26 (0.5 μM-2 μM, 24-72 h) 在 GL261 细胞中升高了 cleaved-PARP (c-PARP) 和 cleaved-caspase-3 (c-caspase 3) 蛋白水平[1]。
ALK-IN-26 (0.5 μM-2 μM, 24-72 h) 在 GL261 细胞中引起凋亡[1]。

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

ALK-IN-26 相关抗体:

Apoptosis Analysis[1]

Cell Line: GL261
Concentration: 0.5 μM, 1.0 μM, 2.0 μM
Incubation Time: 24 h, 48 h, 72 h
Result: Induced apoptosis of glioblastoma in a concentration- and time-dependent manner, and caused the cells (24.5%) entered the S phase but barely proceeded to the G2/M phase when treated with 1 μM for 72 h.

Cell Viability Assay[1]

Cell Line: GL216, U87MG, Hela
Concentration: 0.5 μM, 1.0 μM, 2.0 μM, 5 μM, 10 μM for GL216 and U87MG cells 5 μM, 10 μM, 20 μM, 40 μM, 80 μM, 160 μM for Hela cells
Incubation Time: 24 h, 48h, 72h
Result: Inhibited the activity of GL216 cells with the inhibition rate of cells at 80% when incubated with 2 μM for 72 h and inhibited U87MG cells viability with a dose- and time-dependent manner, while showed limited inhibition on Hela cells, even at 160 μM, the inhibition rate is less than 50%.
Can inhibit the activity of ALK tyrosine kinase with a dose-dependent manner.

Cell Autophagy Assay[1]

Cell Line: GL261
Concentration: 0.5 μM, 1.0 μM, 2.0 μM
Incubation Time: 24 h
Result: Induced autophagy death in glioblastoma cells.
体内研究
(In Vivo)

ALK-IN-26 (5 mg/kg, i.v., 单剂量) 在雄性 C57BL6/J 小鼠中有药代动力学特性[1]。
ALK-IN-26 (20 mg/kg, i.p., 单剂量) 在雄性 C57BL6/J 小鼠中能够穿透血脑屏障[1]。

在雄性小鼠 C57BL6/J 的药代动力学分析[1]

Pharmacokinetic property T1/2(h) Tmax(h) Cmax (ng/mL) AUC(0-8) (h*ng/mL) AUC(0-∞) (h*ng/mL) MRT(0-8) (h) MRT(0-∞) (h) V∞ (L/kg) V2 (L/kg) bioavailablity F (%)
i.v.(5mg/kg) 1.13 0.08 1978.21 884.88 924.56 0.63 0.84 4.59 8.89 38.40
i.p.(5mg/kg) 3.55 0.58 117.57 339.79 420.50 2.25 4.60 / / /

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

Animal Model: Male C57BL/6J mice[1]
Dosage: 5 mg/kg
Administration: Intravenous injection (i.v.), Single dose
Result: Could be rapidly absorbed (Tmax = 0.58 h) with an acceptable half-life (T1/2 = 3.55 h) and bioavailability (F = 38.4%).
Animal Model: Male C57BL/6J mice[1]
Dosage: 20mg/kg
Administration: Intraperitoneal injection (i.p.), Single dose
Result: Could enter the body at concentrations up to 2.7μmol/kg (after 2 h administration at 20 mg/kg) and penetrate the blood-brain barrier.
分子量

405.51

Formula

C24H23NO3S
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

ALK-IN-26 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • 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:

ALK-IN-262447607-85-2Anaplastic lymphoma kinase (ALK)mTORPARPCaspaseAnaplastic lymphoma kinaseALK tyrosine kinase receptorCD246Cluster of differentiation 246Mammalian target of Rapamycinpoly ADP ribose polymeraseGlioblastomaALK modulatorTarget drugU87MGGL261Inhibitorinhibitorinhibit

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