CRM1
- 阻害剤の選択性比較
- 溶解度
| カタログ番号 | 製品カタログ | 溶解度(25°C) | ||
|---|---|---|---|---|
| 水 | DMSO | アルコール | ||
| S7252 | KPT-330 | <1 mg/mL | 88 mg/mL | 40 mg/mL |
| S7125 | KPT-185 | <1 mg/mL | 71 mg/mL | 71 mg/mL |
| S7251 | KPT-276 | <1 mg/mL | 20 mg/mL | <1 mg/mL |
| S8397 | Eltanexor (KPT-8602) | <1 mg/mL | 85 mg/mL | 1 mg/mL |
| S7707 | Verdinexor (KPT-335) | <1 mg/mL | 88 mg/mL | 11 mg/mL |
| S7551 | Piperlongumine | <1 mg/mL | 16 mg/mL | 6 mg/mL |
- CRM1阻害剤(6)
| 製品コード | 製品説明 | 文献中Selleckの製品使用例 | お客様のフィードバック |
|---|---|---|---|
| S7252 |
KPT-330Selinexor (KPT-330) is an orally bioavailable selective CRM1 inhibitor. Phase 2. |
Bortezomib and KPT330 enhance apoptosis in HCT116 and RKO cells. A, HCT116 and RKO cells were treated with bortezomib, KPT330, or their combination for 48 hours at the indicated concentrations. The cells were subsequently stained with Annexin V, apoptotic cells were distinguished by flow cytometric analysis. B, Measurement of caspase-3 and -7 by means of a luminometric assay was performed in cells receiving the same treatment. |
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| S7125 |
KPT-185KPT-185 is a selective CRM1 inhibitor that induces growth inhibition and apoptosis in a panel of NHL cell lines with a median IC50 ~25 nM. |
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| S7251 |
KPT-276KPT-276 is an orally bioavailable selective CRM1 inhibitor. |
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| S8397 |
Eltanexor (KPT-8602)Eltanexor(KPT-8602) is a second-generation, orally bioavailable XPO1 inhibitor with IC50 values of 20−211 nM in 10 AML lines after 3 days exposure. |
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| S7707 |
Verdinexor (KPT-335)Verdinexor (KPT-335) is an orally bioavailable, selective XPO1/CRM1 inhibitor. |
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| S7551 |
PiperlonguminePiperlongumine, a natural alkaloid from Piper longum L., increases the level of reactive oxygen species (ROS) and selectively kills cancer cells. It is a direct TrxR1 inhibitor with suppressive activity against gastric cancer and a novel inhibitor of CRM1; also an inhibitor of PI3K/Akt/mTOR in human breast cancer cells. |
a. Cell growth of ARID1A-wildtype RMG1 cells transfected with ARID1A and non-target siRNA for 24 h and treated with piperlongumine for 72 h. b. Apoptosis of RMG1 cells after transfection and treatment as described in a as measured using annexin-V and PI staining. c. Cell growth of RMG1 cells transfected and treated with 5 μM of piperlongumine as described in a, but in the presence or absence of the antioxidant NAC. Cell growth was measured using the WST-1 assay and quantified relative to DMSO treated non-target control. *P < 0.05; **P < 0.01; ***P < 0.001.
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