CRM1

抑制剂选择性比较

CRM1产品

所有产品 CRM1抑制剂(6)

目录号	产品描述	文献引用	实验数据
S7252	selinexor(KPT-330) Selinexor (KPT-330)是一种口服生物有效的选择性CRM1抑制剂。Phase 2。	Cancers (Basel), 2019, 11(4) Cell Death Dis, 2019, 10(6):395 Neoplasia, 2019, 21(8):788-801	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.
S7125	KPT-185 KPT-185是一种有效的、具有选择性的CRM1抑制剂，可抑制一些NHL细胞的生长并诱导凋亡，IC50约为25 nM。	Exp Cell Res, 2019, 10.1016/j.yexcr.2019.111505 Biochem Biophys Res Commun, 2018, 503(3):1544-1549 Nat Commun, 2017, 8(1):2035	(D)Western blot analysis of RNF146 in cytoplasmic and nuclear fraction after KPT-185 treatment. Data represented mean ± s.e.m., n = 5; P < 0.05, *P < 0.01. NES, nuclear export signal. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
S7251	KPT-276 KPT-276是一种口服生物有效的CRM1选择性抑制剂	Nat Commun, 2019, 10(1):3827 Nature, 2015, 525(7567):56-61
S8397	Eltanexor(KPT-8602) Eltanexor(KPT-8602)是具有口服生物活性的XPO1 (CRM1)抑制剂。在AML细胞系，IC50范围为20-211 nM。	J Cell Mol Med, 2018, 22(12):6099-6111
S7707	Verdinexor（KPT-335） Verdinexor（KPT-335）是一种口服生物可利用的，选择性XPO1/CRM1抑制剂。
S7551	Piperlongumine Piperlongumine，存在于胡椒科植物荜茇中的一种天然生物碱，能够增加reactive oxygen species (ROS)水平，并选择性杀死癌细胞。它还是TrxR1的直接抑制剂，对胃癌具有抑制活性；一种新型的CRM1抑制剂；在人类乳腺癌细胞中可抑制PI3K/Akt/mTOR。	Cancer Cell, 2019, 36(2):179-193 Cell, 2019, 36(2):179-193 Cell Rep, 2019, 28(2):512-525.e6	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.

目录号	产品描述	文献引用	实验数据
S7252	selinexor(KPT-330) Selinexor (KPT-330)是一种口服生物有效的选择性CRM1抑制剂。Phase 2。	Cancers (Basel),2019, 11(4) Cell Death Dis,2019, 10(6):395 Neoplasia,2019, 21(8):788-801	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.
S7125	KPT-185 KPT-185是一种有效的、具有选择性的CRM1抑制剂，可抑制一些NHL细胞的生长并诱导凋亡，IC50约为25 nM。	Exp Cell Res,2019, 10.1016/j.yexcr.2019.111505 Biochem Biophys Res Commun,2018, 503(3):1544-1549 Nat Commun,2017, 8(1):2035	(D)Western blot analysis of RNF146 in cytoplasmic and nuclear fraction after KPT-185 treatment. Data represented mean ± s.e.m., n = 5; P < 0.05, *P < 0.01. NES, nuclear export signal. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
S7251	KPT-276 KPT-276是一种口服生物有效的CRM1选择性抑制剂	Nat Commun,2019, 10(1):3827 Nature,2015, 525(7567):56-61
S8397	Eltanexor(KPT-8602) Eltanexor(KPT-8602)是具有口服生物活性的XPO1 (CRM1)抑制剂。在AML细胞系，IC50范围为20-211 nM。	J Cell Mol Med,2018, 22(12):6099-6111
S7707	Verdinexor（KPT-335） Verdinexor（KPT-335）是一种口服生物可利用的，选择性XPO1/CRM1抑制剂。
S7551	Piperlongumine Piperlongumine，存在于胡椒科植物荜茇中的一种天然生物碱，能够增加reactive oxygen species (ROS)水平，并选择性杀死癌细胞。它还是TrxR1的直接抑制剂，对胃癌具有抑制活性；一种新型的CRM1抑制剂；在人类乳腺癌细胞中可抑制PI3K/Akt/mTOR。	Cancer Cell,2019, 36(2):179-193 Cell,2019, 36(2):179-193 Cell Rep,2019, 28(2):512-525.e6	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.