Umbralisib hydrochloride

Umbralisib hydrochloride (TGR-1202 hydrochloride) 是一种新颖的 PI3Kδ 抑制剂，IC50 和 EC50 值分别为 22.2 nM 和 24.3 nM；Umbralisib hydrochloride (TGR-1202 hydrochloride) 同时可抑制 CK1ε，EC50 值为 6.0 μM。

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库存: 现货

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数量
1mg

￥425.00

340.00

- +
5mg

￥937.00

750.00

- +
10mg

￥1612.00

1290.00

- +
25mg

￥3687.00

2950.00

- +
50mg

￥4862.00

3890.00

- +
100mg

￥8312.00

6650.00

- +

已选 0 种 0 瓶

金额: ￥0.00

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货号: ajce59950
CAS: 1532533-78-0
别名: TGR-1202 hydrochloride; RP5264 hydrochloride
分子式: C31H25ClF3N5O3
分子量: 608.01
纯度: >98%
溶解度: DMSO: ≥ 150 mg/mL (246.71 mM); Water: < 0.1 mg/mL (insoluble)
储存: Store at -20°C
库存: 现货

Background

Umbralisib hydrochloride (TGR-1202 hydrochloride) is a novel PI3Kδ inhibitor, with IC50 and EC50 of 22.2 nM and 24.3 nM, respectively; Umbralisib hydrochloride (TGR-1202 hydrochloride) is also active against CK1ε, with an EC50 value of 6.0 μM. PI3Kδ|22.2 nM (IC50)

Umbralisib (RP5264) causes a half-maximal inhibition of human whole blood CD19 cell proliferation between 100-300 nM[1]. In human lymphoma and leukemia cell lines, Umbralisib (TGR-1202; 10 nM-100 μM) inhibits phosphorylated AKT at Ser473 in a concentration-dependent manner. Umbralisib and carfilzomib synergistically kill blood cancer cells through disrupting the 4E-BP1-eIF4F-c-Myc axis. Umbralisib and carfilzomib in combination synergistically and selectively silence the c-Myc and E2F transcription programs. Umbralisib (15-50 μM) potently represses the expression of c-Myc in the DLBCL cell line LY7, and is uniquely characterized with structural features suitable for targeting CK1ε in lymphoma cells[2].

In a subcutaneous xenograft model of T-cell acute lymphoblastic leukemia (T-ALL) in NOD/SCID mice using the MOLT-4 cell line, Umbralisib (TGR-1202; 150 mg/kg, daily p.o.) significantly shrinks the tumors by day 25[2].

[1]. Swaroop Vakkalankaa, et al. Inhibition of PI3Kδ kinase by a selective, small molecule inhibitor suppresses B-cell proliferation and leukemic cell growth. [2]. Deng C, et al. Silencing c-Myc translation as a therapeutic strategy through targeting PI3Kδ and CK1ε in hematological malignancies. Blood. 2017 Jan 5;129(1):88-99