Atiprimod - CAS 123018-47-3
Catalog number:
123018-47-3
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
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Description:
atiprimod is orally bioavailable small molecule belonging to the azaspirane class of cationic amphiphilic agents with anti-inflammatory, antineoplastic, and antiangiogenic properties. Atiprimod inhibits the phosphorylation of signal transducer and activator of transcription 3 (STAT3), blocking the signalling pathways of interleukin-6 and vascular endothelial growth factor (VEGF) and downregulating the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1, thereby inhibiting cell proliferation, inducing cell cycle arrest, and inducing apoptosis.
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Synonyms:
azaspirane; SKF 106615; SK&F 106615; SK&F-106615.
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Current Developer:
Callisto Pharmaceuticals
1.Combination of atiprimod and the proteasome inhibitor bortezomib induces apoptosis of mantle cell lymphoma in vitro and in vivo.
Sun L1, Zhang L, Qian J, Yang J, Yi Q, Dong W, Wang M. Leuk Res. 2012 Mar;36(3):363-8. doi: 10.1016/j.leukres.2011.09.014. Epub 2011 Oct 13.
The proteasome inhibitor bortezomib (BTZ) is known to be chemotherapeutic in relapsed or refractory mantle cell lymphoma (MCL). Atiprimod (ATI), a novel cationic amphophilic compound, has been tested in clinical trials in multiple myeloma (MM). We sought to evaluate the effect of an ATI-BTZ combination on MCL and to elucidate its therapeutic mechanisms. The ATI and BTZ combination significantly inhibited growth and induced apoptosis of both cultured MCL cell lines and freshly isolated tumor cells from patients with refractory or relapsed MCL. However, the combination yielded lower cytotoxicity in normal peripheral blood mononuclear cells (PBMC). Furthermore, ATI and BTZ induced apoptosis via two different signaling pathways. More significantly, ATI and BTZ markedly delayed tumor growth and prolonged survival in MCL-bearing NOD-SCID mice. Our results demonstrate that ATI and BTZ confer significant therapeutic effects in MCL in vitro and in vivo and should therefore be investigated in a clinical trial in patients with relapsed or refractory MCL.
2.A severe combined immunodeficient-hu in vivo mouse model of human primary mantle cell lymphoma.
Wang M1, Zhang L, Han X, Yang J, Qian J, Hong S, Lin P, Shi Y, Romaguera J, Kwak LW, Yi Q. Clin Cancer Res. 2008 Apr 1;14(7):2154-60. doi: 10.1158/1078-0432.CCR-07-4409.
PURPOSE: To establish a severe combined immunodeficient (SCID)-hu in vivo mouse model of human primary mantle cell lymphoma (MCL) for the study of the biology and novel therapy of human MCL.
3.Atiprimod inhibits the growth of mantle cell lymphoma in vitro and in vivo and induces apoptosis via activating the mitochondrial pathways.
Wang M1, Zhang L, Han X, Yang J, Qian J, Hong S, Samaniego F, Romaguera J, Yi Q. Blood. 2007 Jun 15;109(12):5455-62. Epub 2007 Feb 22.
Atiprimod is a novel cationic amphiphilic compound and has been shown to exert antimyeloma effects both in vitro and in mouse experiments. This study was undertaken to evaluate the therapeutic efficacy of atiprimod on mantle cell lymphoma (MCL) and elucidate the mechanism by which it induces cell apoptosis. Atiprimod inhibited the growth and induced apoptosis of MCL cell lines and freshly isolated primary tumor cells in vitro. More importantly, atiprimod significantly inhibited tumor growth in vivo and prolonged the survival of tumor-bearing mice. However, atiprimod also exhibited lower cytotoxicity toward normal lymphocytes. Atiprimod activated c-Jun N-terminal protein kinases (JNK) and up-regulated the level of Bax, Bad, and phosphorylated Bcl-2, resulting in release of apoptosis-inducing factor (AIF) and cytochrome c from mitochondria and activation and cleavage of caspase-9, caspase-3, and PARP. However, AIF, but not activation of caspases or PARP, was responsible for apoptosis in MCL cells because an AIF inhibitor, but not pan-caspase or paspase-9 inhibitors, completely abrogated atiprimod-induced apoptosis.
4.Efficient approach to the Azaspirane core of FR 901483.
Kaden S1, Reissig HU. Org Lett. 2006 Oct 12;8(21):4763-6.
[reaction: see text] An efficient approach to the azaspirane core of FR 901483 is described employing lithiated methoxyallene as a crucial C3 building block and a suitably protected enantiopure ketimine as the second component. The resulting dihydropyrrole derivative was smoothly converted into a spiro keto aldehyde which under acidic conditions provided a novel azanorbornane derivative 15. Under basic reaction conditions, the desired 5-azatricyclo[6.3.1.0(1,5)]dodecane skeleton 16 was generated. The ratio of diastereomers strongly depends on the reaction conditions employed with l-proline in DMSO providing the highest selectivity in favor of one azaspirane product.
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CAS 123018-47-3 Atiprimod

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