5388-21-6

Usage

Uses

Used in Pharmaceutical Industry:
5-Pyrimidinecarboxylic acid, 2-(methylamino)(7CI,8CI,9CI) is utilized as a key intermediate in the synthesis of various pharmaceuticals for its unique structural properties that can be incorporated into drug molecules to enhance their therapeutic effects.
Used in Organic Synthesis:
As a building block, 5-Pyrimidinecarboxylic acid, 2-(methylamino)(7CI,8CI,9CI) is employed in organic synthesis to create a range of chemical compounds, leveraging its pyrimidine ring and functional groups for the development of new molecules with specific applications.
Further Research:
5-Pyrimidinecarboxylic acid, 2-(methylamino)(7CI,8CI,9CI) is a subject of ongoing research to fully explore and understand its potential applications and effects in various fields, including medicinal chemistry and materials science. This research aims to uncover new uses and optimize its synthesis for industrial applications.

InChI:InChI=1/C6H7N3O2/c1-7-6-8-2-4(3-9-6)5(10)11/h2-3H,1H3,(H,10,11)(H,7,8,9)

Upstream product

• 1581701-20-3 methyl 2-(methylamino)pyrimidine-5-carboxylate 
• 31402-54-7 5-bromo-N-methylpyrimidin-2-amine 

Downstream Products

• 1581701-26-9 N-(2-methyl-5-((4-((4-methylpiperazin-1-yl)methyl)-3-(trifluoromethyl)phenyl)carbamoyl)phenyl)-2-(methylamino)pyrimidine-5-carboxamide 

Relevant academic research and scientific papers

Identification and optimization of new dual inhibitors of B-Raf and epidermal growth factor receptor kinases for overcoming resistance against vemurafenib

Epidermal growth factor receptor (EGFR) amplification has been demonstrated to be critical for the inherent and/or acquired resistance against current B-RafV600E inhibitor therapy for melanoma and colorectal cancer patients. We describe the discovery and structure-activity relationship study of a series of 1H-pyrazolo[3,4-b]pyridine-5-carboxamide analogues as novel dual inhibitors of EGFR and B-RafV600E mutant. One of the most promising compounds, 6a, potently inhibited both of the kinases with IC50 values of 8.0 and 51 nM, respectively. The compound also strongly suppressed the proliferation of a panel of intrinsic and acquired resistant melanoma and/or colorectal cancer cells harboring overexpressed EGFR with submicromolar IC 50 values. Further mechanism investigation revealed that 6a could sustainably inhibit the activation of the MAPK path way in the resistant SK-MEL-28 PR30 melanoma cancer cells and WiDr colorectal cancer cells with EGFR amplification. Our results support the hypothesis that the EGFR/B-Raf V600E dual inhibition might be a tractable strategy to overcome the intrinsic and acquired resistance of melanoma and/or colorectal cancers against the current B-RafV600E inhibitor therapy.