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Submit ReviewCFM 4
Description: CARP-1 mimetic; proapoptotic
Chemical Name: 1-[(2-Chlorophenyl)methyl]-5'-phenyl-spiro[3H-indole-3,2'(3'H)-[1,3,4]thiadiazol]-2(1H)-one
Purity: ≥99% (HPLC)
Biological Activity for CFM 4
CFM 4 is a CARP-1 mimetic; interferes with CARP-1 binding to APC-2. Enhances CARP-1 expression and induces G2/M cell cycle arrest. Induces apoptosis and suppresses cell growth in cancer cells.
Technical Data for CFM 4
| M. Wt | 405.9 |
| Formula | C22H16ClN3OS |
| Storage | Store at +4°C |
| Purity | ≥99% (HPLC) |
| CAS Number | 331458-02-7 |
| PubChem ID | 2871439 |
| InChI Key | PMADITKBVODKSF-UHFFFAOYSA-N |
| Smiles | O=C2N(CC4=CC=CC=C4Cl)C1=CC=CC=C1C32NN=C(C5=CC=CC=C5)S3 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Product Datasheets for CFM 4
References for CFM 4
References are publications that support the biological activity of the product.
Puliyappadamba et al (2011) Antagonists of anaphase-promoting complex (APC)-2-cell cycle and apoptosis regulatory protein (CARP)-1 interaction are novel regulators of cell growth and apoptosis. J.Biol.Chem. 286 38000 PMID: 21903591
Ashour et al (2013) CARP-1 functional mimetics: a novel class of small molecule inhibitors of medulloblastoma cell growth. PLoS ONE 8 e66733 PMID: 23826121
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Keywords: CFM 4, CFM 4 supplier, CFM4, CARP-1, mimetic, proapoptotic, antitumor, antitumorgenic, APC-2, G2M, cell, cycle, arrest, Apoptosis, Inducers, Cell, Cycle, Inhibitors, 5144, Tocris Bioscience
Citations for CFM 4
Citations are publications that use Tocris products.
Currently there are no citations for CFM 4.
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Literature in this Area
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.
Pathways for CFM 4
