123018-47-3
Chemical Structure
Atiprimod
Synonym(s): Azaspirane ; SKF 106615-12; SKF 106615A12
- CAS No.: 123018-47-3
- Formula:C22H44N2
- Molecular Weight:336.60
IUPAC Name: 3-(8,8-dipropyl-2-azaspiro[4.5]decan-2-yl)-N,N-diethylpropan-1-amine
InChIKey: SERHTTSLBVGRBY-UHFFFAOYSA-N
SMILES: CCN(CCCN1CCC2(CCC(CCC)(CC2)CCC)C1)CC
Biological Activity: Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML)[1][2][3][4][5][6].
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Atiprimod | Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML). | |||||||||||||||||||||
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- [1]. Coker-Gurkan A, et al. Atiprimod induce apoptosis in pituitary adenoma: Endoplasmic reticulum stress and autophagy pathways. J Cell Biochem. 2019 Dec;120(12):19749-19763. [Content Brief]
- [2]. Coker-Gurkan A, et al Atiprimod triggered apoptotic cell death via acting on PERK/eIF2α/ATF4/CHOP and STAT3/NF-ΚB axis in MDA-MB-231 and MDA-MB-468 breast cancer cells. Mol Biol Rep. 2021 Jun;48(6):5233-5247. [Content Brief]
- [3]. Faderl S, et al. Atiprimod blocks phosphorylation of JAK-STAT and inhibits proliferation of acute myeloid leukemia (AML) cells. Leuk Res. 2007 Jan;31(1):91-5. [Content Brief]
- [4]. Wang M, et al. Atiprimod inhibits the growth of mantle cell lymphoma in vitro and in vivo and induces apoptosis via activating the mitochondrial pathways. Blood. 2007 Jun 15;109(12):5455-62. [Content Brief]
- [5]. Hamasaki M, et al. Azaspirane (N-N-diethyl-8,8-dipropyl-2-azaspiro [4.5] decane-2-propanamine) inhibits human multiple myeloma cell growth in the bone marrow milieu in vitro and in vivo. Blood. 2005 Jun 1;105(11):4470-6. [Content Brief]
- [6]. Quintás-Cardama A, et al. Preclinical characterization of atiprimod, a novel JAK2 AND JAK3 inhibitor. Invest New Drugs. 2011 Oct;29(5):818-26. [Content Brief]
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