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SML1212

Sigma-Aldrich

CPI203

≥98% (HPLC)

Synonyme(s) :

(6S)-4-(4-Chlorophenyl)-2,3,9-trimethyl-6H-thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine-6-acetamide

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About This Item

Formule empirique (notation de Hill):
C19H18ClN5OS
Numéro CAS:
1446144-04-2
Poids moléculaire :
399.90
Numéro MDL:
MFCD27997886
Code UNSPSC :
12352200
ID de substance PubChem :
329825722
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 20 mg/mL, clear

Température de stockage

2-8°C

Chaîne SMILES 

CC1=NN=C2[C@H](CC(N)=O)N=C(C3=CC=C(Cl)C=C3)C4=C(SC(C)=C4C)N21

InChI

1S/C19H18ClN5OS/c1-9-10(2)27-19-16(9)17(12-4-6-13(20)7-5-12)22-14(8-15(21)26)18-24-23-11(3)25(18)19/h4-7,14H,8H2,1-3H3,(H2,21,26)/t14-/m0/s1

Clé InChI

QECMENZMDBOLDR-AWEZNQCLSA-N

Actions biochimiques/physiologiques

CPI203 is an analog of the BET inhibitor (BETi) (+)-JQ1 and is bioavailable via oral or intraperitoneal administration. It plays an important role in lenalidomide and dexamethasone functions in in vitro and in vivo models of multiple myeloma. CPI203 inhibits proliferation, apoptosis and cell cycle arrest in A431 cell line and primary skin squamous cell carcinoma (SCC) cells.
CPI203 is an inhibitor of BRD4, a bromodomain-containing protein that binds to histones to regulate recruitment of transcription factors. BRD4 is also an RNA Pol II kinase. CPI203 blocks BRD4 kinase activity in cells and in vivo. It has shown synergistic antitumor activity with lenalidomide in bortezomib-resistant mantle cell lymphoma.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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Bromodomain protein BRD4 promotes cell proliferation in skin squamous cell carcinoma.
Xiang T, et al.
Cellular Signalling, 42, 106-113 (2018)
The BET bromodomain inhibitor CPI203 improves lenalidomide and dexamethasone activity in in vitro and in vivo models of multiple myeloma by blockade of Ikaros and MYC signaling.
Diaz T, et al.
Haematologica, 102(10), 1776?1784-1776?1784 (2017)
Yutuan Wu et al.
Journal of cancer research and clinical oncology, 148(4), 803-821 (2022-01-31)
Tumor-associated macrophages (TAMs) are known to contribute to adaptive resistance to anti-vascular endothelial growth factor (VEGF) antibody (AVA) therapy in ovarian cancer. BET (bromodomain and extra-terminal domain) inhibitors (BETi) may have unique roles in targeting TAMs. Our objective was to
Lisa-Maria Winter et al.
Scientific reports, 13(1), 12061-12061 (2023-07-27)
GDF15 has recently emerged as a key driver of the development of various disease conditions including cancer cachexia. Not only the tumor itself but also adverse effects of chemotherapy have been reported to contribute to increased GDF15. Although regulation of
Masao Nakagawa et al.
Cancer cell, 34(2), 286-297 (2018-07-31)
Adult T cell leukemia/lymphoma (ATLL) is a frequently incurable disease associated with the human lymphotropic virus type I (HTLV-I). RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression. HBZ, the
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