60284-53-9

Upstream product

• 625-36-5 2-chloropropionyl chloride 
• 99-09-2 3-nitro-aniline 

Downstream Products

• 854904-22-6 N-(3-nitrophenyl)-3-(piperidin-1-yl)propanamide 
• 88858-79-1 3-(diethylamino)-N-(3-nitrophenyl)propanamide 
• 38560-29-1 N-(m-nitrophenyl)-β-lactam 
• 851651-86-0 N-(3-nitrophenyl)-3-(pyrrolidin-1-yl)propanamide 
• 1233488-29-3 C₁₁H₁₁N₅O₃S 
• 1444512-05-3 diethyl [N-(3-nitrophenyl)carbamoyl]ethylphosphonate 
• 1446421-40-4 3-(dimethylamino)-N-(3-nitrophenyl)propanamide 
• 1586764-64-8 3-morpholino-N-(3-nitrophenyl)propanamide 
• 52029-87-5 N-<3-Chlor-propionyl>-m-phenylendiamin 
• 1616381-19-1 N-{3-[(2-chloro-5-fluoropyrimidin-4-yl)amino]phenyl}prop-2-enamide 
• 1070978-30-1 5,5'-ureylene-di-(1-(3-(3-(pyrrolidin-1-yl)propanamido)-phenyl)-3-phenylurea) 
• 1070978-46-9 1,3-bis(4-(1-(3-(3-(pyrrolidin-1-yl)propanamido)phenyl)-1H-1,2,3-triazol-4-yl)phenyl)urea 
• 1070977-78-4 1,3-bis(3-(3-(3-(pyrrolidin-1-yl)propanamido)phenylcarbamoyl)phenyl)urea 

Relevant academic research and scientific papers

Design, synthesis, and biological evaluation of hydroxamic acid-substituted 2,4-diaryl aminopyrimidines as potent EGFRT790M/L858R inhibitors for the treatment of NSCLC

A series of 2,4-diarylaminopyrimidine derivatives bearing hydrophilic hydroxamic acids were designed and synthesized as potent EGFRT790M/L858R inhibitors. Among the derivatives synthesized, 10c (IC50 = 5.192 nM), 10j (IC50 = 10.35 nM), and 10o (IC50 = 0.3524 nM) exhibited higher potencies against EGFRT790/M/L858R compared to the known EGFR inhibitor AZD-9291 (IC50 = 20.80 nM). Moreover, 10j showed moderate activity against H1975 cells transfected with the EGFRT790M/L858R mutant, with an IC50 of 0.2113 μM over A431 (wild-type EGFR, SI = 47.3). In addition, 10j exhibited low toxicity in normal HBE cells (human bronchial epithelial cells, IC50 > 40 μΜ). Analysis of the mode of action indicated that 10j effectively induced apoptosis in H1975 cells by arresting the cells in the G2/M phase. Compound 10j also demonstrated efficacy in inhibiting tumor growth in a H1975 xenograft mouse model without losing body weight or killing the mice. Taken together, these results suggested that 10j might be a promising candidate for development as a potential treatment for NSCLC harboring the EGFRT790M/L858R mutation.

Synthesis and antimalarial activity of N-benzylated (N-arylcarbamoyl)alkylphosphonic acid derivatives

A series of novel and readily accessible N-benzylated (N-arylcarbamoyl)alkylphosphonate esters and related compounds have been prepared as potential antimalarial agents. Bioassays reveal that some of these compounds exhibit promising activity against Plasmodium falciparum, and exhibit no significant growth inhibition of HeLa cells.

Design and synthesis of potent antitumor water-soluble phenyl N-mustard-benzenealkylamide conjugates via a bioisostere approach

A series of new, water-soluble phenyl N-mustard-benzenealkylamide conjugates containing hydrophilic ω-dialkylaminoalkylamide or ω-cyclic aminoalkylamide moieties were synthesized via a bioisostere approach. These compounds have a broad spectrum of antitumor activity against a panel of human tumor cell lines. Of these derivatives, compound 18b effectively suppressed the growth of colon cancer (HCT-116), prostate cancer (PC3), and lung cancer (H460) xenografts. The growth of HCT-116 xenografts was almost completely suppressed when co-treated with compound 18b and 5-fluorouracil. Furthermore, compound 18b can induce DNA cross-linking and cell-cycle arrest at the G2/M phase. Early preclinical studies, including pharmacokinetics in rats, inhibition of the hERG, and 14 days of acute intravenous injection toxicity, suggest that compound 18b is a promising candidate for further preclinical studies.

Exploring DOXP-reductoisomerase binding limits using phosphonated N-aryl and N-heteroarylcarboxamides as DXR inhibitors

DOXP-reductoisomerase (DXR) is a validated target for the development of antimalarial drugs to address the increase in resistant strains of Plasmodium falciparum. Series of aryl- and heteroarylcarbamoylphosphonic acids, their diethyl esters and disodium salts have been prepared as analogues of the potent DXR inhibitor fosmidomycin. The effects of the carboxamide N-substituents and the length of the methylene linker have been explored using in silico docking studies, saturation transfer difference NMR spectroscopy and enzyme inhibition assays using both EcDXR and PfDXR. These studies indicate an optimal linker length of two methylene units and have confirmed the importance of an additional binding pocket in the PfDXR active site. Insights into the constraints of the PfDXR binding site provide additional scope for the rational design of DXR inhibitors with increased ligand-receptor interactions.

Synthesis and biological screening of novel derivatives of 3-(N-substituted carboxamidoethylthio)-(4H)-1,2,4-triazoles

3-Mercapto-(4H)-1,2,4-triazole has been synthesized from 1-formylthiosemicarbazide. Different N-substituted β-chloropropionamides have been prepared by reacting substituted amines with β- chloropropionylchloride. Different Nsubstituted β-chloropropionamides have been condensed with 3-mercapto-(4H)-1,2,4-triazole in basic medium to obtain various 3-(N-substituted carboxamidoethylthio)-(4H)-1,2,4-triazoles. The structure of the synthesized compounds are confirmed by IR, 1H NMR spectra and elemental analysis. All the compounds have been screened for their analgesic, anti-inflammatory and anxiolytic activity.

Design, synthesis and evaluation of 4,5-di-substituted acridone ligands with high G-quadruplex affinity and selectivity, together with low toxicity to normal cells

A series of 4,5-di-substituted acridones have been designed and synthesized. Several compounds show high affinity for telomeric G-quadruplex DNA in classical and competition FRET assays, together with low duplex DNA affinity, although they do not show activity in a telomerase assay or evidence of telomere shortening. They have low toxicity against a panel of cancer cell lines and a normal human fibroblast line, and produce potent senescence-based long-term growth arrest in the MCF7 and A549 cancer cell lines.

Rational design of substituted diarylureas: A scaffold for binding to G-quadruplex motifs

The design and synthesis of a series of urea-based nonpolycyclic aromatic ligands with alkylaminoanilino side chains as telomeric and genomic G-quadruplex DNA interacting agents are described. Their interactions with quadruplexes have been examined by means of fluorescent resonance energy transfer melting, circular dichroism, and surface plasmon resonance-based assays. These validate the design concept for such urea-based ligands and also show that they have significant selectivity over duplex DNA, as well as for particular G-quadruplexes. The ligand-quadruplex complexes were investigated by computational molecular modeling, providing further information on structure-activity relationships. Preliminary biological studies using short-term cell growth inhibition assays show that some of the ligands have cancer cell selectivity, although they appear to have low potency for intracellular telomeric G-quadruplex structures, suggesting that their cellular targets may be other, possibly oncogene-related quadruplexes.

UREYLENE DERIVATIVES

The invention concerns compounds of Formula (I) or a salt, solvate or pro-drug thereof. The compounds may be used in therapy, particularly anti-cancer therapy.

Click chemistry assembly of G-quadruplex ligands incorporating a diarylurea scaffold and triazole linkers

A series of diarylurea ligands were designed to interact selectively with G-quadruplexes and were synthesised using copper(I) catalysed 'click' chemistry to incorporate the 1,4-substituted 1,2,3-triazole ring into the core of the ligands; the optimal ligands demonstrate a high degree of selective telomeric G-quadruplex stabilisation and are not cytotoxic in several cancer cell lines. The Royal Society of Chemistry.

Herbicidal N-aryl substituted azetidinones

Disclosed are herbicidal compositions comprising an inert carrier and as an essential active ingredient in a quantity toxic to weeds a compound of the formula EQU1 wherein X is selected from the group consisting of alkyl, alkenyl, alkoxy, alkylthio, halogen, haloalkyl and nitro; and n is an integer from 0 to 5.