89479-61-8

Basic information

• Product Name: Glycine, N-cyclopentyl-, ethyl ester
• Synonyms: Glycine, N-cyclopentyl-, ethyl ester
• CAS NO: 89479-61-8
• Molecular Formula: C₉H₁₇NO₂
• Molecular Weight: 171.23678
• Mol File: 89479-61-8.mol
• Article Data: 6

Chemical Properties

• Appearance: /
• CAS DataBase Reference: Glycine, N-cyclopentyl-, ethyl ester(CAS DataBase Reference)
• NIST Chemistry Reference: Glycine, N-cyclopentyl-, ethyl ester(89479-61-8)
• EPA Substance Registry System: Glycine, N-cyclopentyl-, ethyl ester(89479-61-8)

Safety Data

• Hazardous Substances Data: 89479-61-8(Hazardous Substances Data)

Upstream product

• 105-36-2 ethyl bromoacetate 
• 1003-03-8 Cyclopentamine 
• 623-33-6 glycine ethyl ester hydrochloride 
• 120-92-3 cyclopentanone 

Downstream Products

• 92399-73-0 ethyl N-(2-acetoxy-3,5-dichlorobenzoyl)-N-cyclopentylglycinate 
• 1374639-78-7 N,N‐dimethyl‐7‐cyclopentyl‐2‐{[5‐(4-tert-butoxycarbonylpiperazin‐1‐yl)pyridin‐2‐yl]amino}‐7H‐pyrrolo[2,3‐d]pyrimidine‐6‐carboxamide 
• 84126-69-2 N-cyclopentyl glycine ethyl ester hydrochloride 
• 172834-23-0 N^α-Boc-N-cyclopentylglycine 
• 89479-63-0 ethyl N-(3-chloro-2-mercaptobenzoyl)-N-cyclopentylglycinate 
• 83596-90-1 N-(3-chloro-2-mercaptobenzoyl)-N-cyclopentylglycine 
• 131565-80-5 4-(4-Chloro-benzenesulfonylaminocarbonyl)-N-((S)-1-{cyclopentyl-[(3,3,3-trifluoro-1-isopropyl-2-oxo-propylcarbamoyl)-methyl]-carbamoyl}-2-methyl-propyl)-benzamide 
• 131506-19-9 4-(4-Chloro-benzenesulfonylaminocarbonyl)-N-((S)-1-{cyclopentyl-[(3,3,3-trifluoro-2-hydroxy-1-isopropyl-propylcarbamoyl)-methyl]-carbamoyl}-2-methyl-propyl)-benzamide 

Relevant articles and documents

Alkali-metal hexamethyldisilazide initiated polymerization on alpha-amino acid N-substituted N-carboxyanhydrides for facile polypeptoid synthesis

Polypeptoids have been explored as mimics of polypeptides, owing to polypeptoids’ superior stability upon proteolysis. Polypeptoids can be synthesized from one-pot ring-opening polymerization of amino acid N-substituted N-carboxyanhydrides (NNCAs). However, the speed of polymerization of NNCAs can be very slow, especially for NNCAs bearing a bulky N-substitution group. This hindered the exploration on polypeptoids with more diverse structures and functions. Therefore, it is in great need to develop advanced strategies that can accelerate the polymerization on inactive NNCAs. Hereby, we report that lithium/sodium/potassium hexamethyldisilazide (Li/Na/KHMDS) initiates a substantially faster polymerization on NNCAs than do commonly used amine initiators, especially for NNCAs with bulky N-substitution group. This fast NNCA polymerization will increase the structure diversity and application of polypeptoids as synthetic mimics of polypeptides.

Synthetic method of cyclopentyl pyrimido pyrroles compound

The invention discloses a synthetic method of a cyclopentyl pyrimido pyrroles compound, which belongs to the field of organic chemical synthesis. Through steps of reduction, oxidation, aldol condensation, aminolysis and nucleophilic substitution, the cyclopentyl pyrimido pyrroles compound is synthesized. The raw materials have the advantages of low cost and easy acquisition, a related intermediate is easily separated and purified, operation is simple, the method is friendly to environment, the purity of the product is high, and the product has good industrial prospect. The prepared cyclopentyl pyrimido pyrroles compound, especially 7-cyclopentyl-N,N-dimethyl-2-((5-(piperazine-1-yl)pyridine-2-yl)amino)-7H-pyrrolo[2,3-d]pyrimidine-6-methanamide has inhibition effect on cyclin-dependent kinase CDK4/6, and has good clinical treatment effect on melanoma and breast cancer.

Inhibition of human leukocyte elastase (HLE) by N-substituted peptidyl trifluoromethyl ketones

A series of tripeptides possessing trifluoromethyl or aryl ketone residues at P1 were prepared and evaluated both in vitro and in vivo as potential inhibitors of human leukocyte elastase (HLE). Tripeptides containing non naturally occurring N-substituted glycine residues at the P2-position have been demonstrated to be potent in vitro inhibitors of HLE, with IC50 values in the submicromolar range. Sterically demanding substituents on the P2- nitrogen have no detrimental effect on in vitro potency. The inhibition process presumably acts via hemiketal formation with the active site Ser195 of HLE, and is facilitated by the strongly electron withdrawing trifluoromethyl functionality. Deletion of the amino acid at the P3-subsite region affords inactive compounds. Valine is the preferred residue at the P1-position, whereas the corresponding glycine, alanine, α,α- dimethylglycine, or phenylalanine analogues are all inactive. The compounds described herein all confer a high degree of in vitro specificity when tested against representative cysteine, aspartyl, metallo, and other serine proteases. One of the most potent in vitro inhibitors is (3RS)-N-[4[[[(4- chlorophenyl)sulfonyl]amino]carbonyl]phenyl]oxomethyl]-L-valyl-N-(2,3- dihydro-1H-inden-2-yl)glycine N-[3-(1,1,1-trifluoro-4-methyl-2- oxopentyl)amide (20i; BI-RA-260) (IC50 = 0.084 μM). Compound 20i was also tested in hamsters in an elastase-induced pulmonary hemorrhage (EPH) model. In this model, intratracheal (it.) administration of 20i, 5 min prior to HLE challenge, effectively inhibited hemorrhage in a dose-dependent manner with an ED50 of 4.8 μg. The inhibitor 20i, 20 μg administered it. 24, 48, and 72 h prior to HLE challenge, exhibits significant inhibition against hemorrhage at all time points (97%, 64% and 49%, respectively). In a 21-day chronic model of emphysema in hamsters, 200 μg of HLE administered it. caused an elastase-induced emphysema in the lungs which can be quantitated histologically utilizing image analysis. In this assay, 20i significantly inhibited pulmonary lesions associated with septal destruction and increased alveolar spaces, when dosed at 20 μg it. 5 min prior to challenge with HLE.