PRIMA-1MET
Chemical Name: 2-(Hydroxymethyl)-2-(methoxymethyl)-1-azabicyclo[2.2.2]octan-3-one
Purity: ≥98%
Biological Activity
PRIMA-1MET is a methylated derivative of PRIMA-1 (Cat. No. 1862). Restores mutant activity p53 activity. Acts synergistically with chemotherapeutic agents to inhibit tumor cell proliferation.Technical Data
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.
Background References
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Variability in functional p53 reactivation by PRIMA-1(Met)/APR-246 in Ewing sarcoma.
Aryee, D N T, Niedan, S, Ban, J, Schwentner, R, Muehlbacher, K, Kauer, M, Kofler, R, Kovar, H
Br J Cancer, 2013;109(10):2696-704. -
RB1 status in triple negative breast cancer cells dictates response to radiation treatment and selective therapeutic drugs.
Robinson T, Liu J, Vizeacoumar F, Sun T, Maclean N, Egan S, Schimmer A, Datti A, Zacksenhaus E
PLoS ONE, 2013;8(11):e78641. -
PRIMA-1MET induces mitochondrial apoptosis through activation of caspase-2.
Shen et al.
Oncogene, 2008;27:6571 -
PRIMA-1MET induces nucleolar translocation of Epstein-Barr virus-encoded EBNA-5 protein.
Stuber et al.
Mol.Cancer, 2009;8:23 -
PRIMA-1MET synergizes with cisp. to induce tumor cell apoptosis.
Bykov et al.
Oncogene, 2005;24:3484
Product Datasheets
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Citations for PRIMA-1MET
The citations listed below are publications that use Tocris products. Selected citations for PRIMA-1MET include:
3 Citations: Showing 1 - 3
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Ovarian Cancers with Low CIP2A Tumor Expression Constitute an APR-246-Sensitive Disease Subtype.
Authors: Katja Et al.
Mol Cancer Ther 2022;21:1236-1245
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Estrogen Receptor-Beta2 (ERβ2)-Mutant p53-FOXM1 Axis: A Novel Driver of Proliferation, Chemoresistance, and Disease Progression in High Grade Serous Ovarian Cancer (HGSOC).
Authors: Kunle O Et al.
Cancers (Basel) 2022;14
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RB1 status in triple negative breast cancer cells dictates response to radiation treatment and selective therapeutic drugs.
Authors: Robinson Et al.
PLoS One 2013;8:e78641
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