173458-77-0

Upstream product

• 64-18-6 formic acid 
• 55817-72-6 2-amino-1-benzyl-4,5-dimethyl-1H-pyrrole-3-carbonitrile 
• 513-86-0 3-hydroxy-2-butanon 
• 100-46-9 benzylamine 
• 109-77-3 malononitrile 
• 1395346-62-9 2-amino-1-benzyl-4,5-dimethyl-1H-pyrrole-3-carboxamide 
• 109-94-4 formic acid ethyl ester 

Downstream Products

• 173458-80-5 7-benzyl-4-chloro-5,6-dimethyl-7H-pyrrolo[2,3-d]pyrimidine 
• 173458-79-2 7-benzyl-5,6-diphenyl-7H-pyrrolo[2,3-d]pyrimidin-4-ol 
• 173458-86-1 (7-Benzyl-5,6-dimethyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl)-(3,5-dichloro-phenyl)-amine 
• 1027236-75-4 (7-Benzyl-5,6-dimethyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl)-(3-chloro-phenyl)-methyl-amine 
• 173458-84-9 4-(m-Bromoanilino)-5,6-dimethyl-7-benzyl-pyrrolo[2,3-d]pyrimidine 
• 173458-83-8 4-(m-chloroanilino)-5,6-dimethyl-7-benzyl-pyrrolo[2,3-d]pyrimidine 
• 173458-85-0 4-(m-Fluoroanilino)-5,6-dimethyl-7-benzyl-pyrrolo[2,3-d]pyrimidine 

Relevant academic research and scientific papers

Discovery and Optimization of Pyrrolopyrimidine Inhibitors of Interleukin-1 Receptor Associated Kinase 4 (IRAK4) for the Treatment of Mutant MYD88L265P Diffuse Large B-Cell Lymphoma

Herein we report the optimization of a series of pyrrolopyrimidine inhibitors of interleukin-1 receptor associated kinase 4 (IRAK4) using X-ray crystal structures and structure based design to identify and optimize our scaffold. Compound 28 demonstrated a favorable physicochemical and kinase selectivity profile and was identified as a promising in vivo tool with which to explore the role of IRAK4 inhibition in the treatment of mutant MYD88L265P diffuse large B-cell lymphoma (DLBCL). Compound 28 was shown to be capable of demonstrating inhibition of NF-κB activation and growth of the ABC subtype of DLBCL cell lines in vitro at high concentrations but showed greater effects in combination with a BTK inhibitor at lower concentrations. In vivo, the combination of compound 28 and ibrutinib led to tumor regression in an ABC-DLBCL mouse model.

Rapid and efficient, microwave-assisted, base-catalyzed synthesis of some novel 2,7-disubstituted pyrrolopyrimidinones

A rapid synthesis of a series of new 5,6-dimethyl-7-phenyl-2-alkyl-3,7- dihydro-4H-pyrrolo[2,3-d]pyrimidinones and 5,6-dimethyl-7-benzyl-2-alkyl-3,7- dihydro-4H-pyrrolo[2,3-d]pyrimidinones was accomplished in good yields using microwave irradiation under

PYRROLOPYRIMIDINES FOR PHARMACEUTICAL COMPOSITIONS

The present invention relates to novel pyrrolopyrimidine compounds and pharmaceutical compositions comprising said pyrrolopyrimidine compounds. Moreover, the present invention relates to the use of the pyrrolopyrimidine compounds of the invention for the

4-(Phenylamino)pyrrolopyrimidines: Potent and selective, ATP site directed inhibitors of the EGF-receptor protein tyrosine kinase

Using a pharmacophore model for ATP-competitive inhibitors interacting with the active site of the EGF-R protein tyrosine kinase (PTK), 4- (phenylamino)-7H-pyrrolo[2,3-d]pyrimidines have been identified as a novel class of potent EGF-R protein tyrosine kinase inhibitors. In an interactive process, this class of compounds was then optimized. 13, 14, 28, 36, 37, and 44, the most potent compounds of this series, inhibited the EGF-R PTK with IC50 values in the low nanomolar range. High selectivity toward a panel of nonreceptor tyrosine kinases (c-Src, v-Abl) and serine/threonine kinases (PKC α, PKA) was observed. Kinetic analysis revealed competitive type kinetics relative to ATP. In cells, EGF-stimulated cellular tyrosine phosphorylation was inhibited by compounds 13, 36, 37, and 44 at IC50 values between 0.1 and 0.4 μM, whereas PDGF-induced tyrosine phosphorylation was not affected by concentrations up to 10 μM. In addition, these compounds were able to selectively inhibit c-fos mRNA expression in EGF-dependent cell lines with IC50 values between 0.1 and 2 μM, but did not affect c-fos mRNA induction in response to PDGF or PMA (IC50 >100 μM). Proliferation of the EGF- dependent MK cell line was inhibited with similar IC50 values. From SAR studies, a binding mode for 4-(phenylamino)-7H-pyrrolo[2,3-d]pyrimidines as well as for the structurally related 4-(phenylamino)quinazolines at the ATP- binding site of the EGF-R tyrosine kinase is proposed. 4-(Phenylamino)-7H- pyrrolo[2,3-d]pyrimidines therefore represent a new class of highly potent tyrosine kinase inhibitors which preferentially inhibit the EGF-mediated signal transduction pathway and have the potential for further evaluation as anticancer agents.