42435-88-1

Usage

Uses

Used in Pharmaceutical Industry:
L-Proline, 1-methyl-5-oxo-, methyl ester (9CI) is used as a pharmaceutical intermediate for the development of drugs targeting various health conditions. The unique structural features of L-Proline, 1-methyl-5-oxo-, methyl ester (9CI) may offer novel therapeutic avenues, such as modulating protein synthesis or interacting with specific biological targets.
Used in Agricultural Industry:
In agriculture, L-Proline, 1-methyl-5-oxo-, methyl ester (9CI) may serve as a component in the formulation of biostimulants or plant growth regulators. Its role in protein synthesis could potentially enhance plant growth and stress resistance, contributing to improved crop yields and quality.
Used in Materials Science:
L-Proline, 1-methyl-5-oxo-, methyl ester (9CI) is utilized in the development of novel materials with specific properties. L-Proline, 1-methyl-5-oxo-, methyl ester (9CI)'s unique chemical structure may contribute to the creation of advanced materials with applications in various industries, such as biodegradable plastics or smart materials that respond to environmental stimuli.
Note: The specific applications mentioned above are hypothetical and provided as examples based on the general properties of L-Proline, 1-methyl-5-oxo-, methyl ester (9CI). Actual uses may vary and require further research and development.

Upstream product

• 98-79-3 L-Pyroglutamic acid 
• 74-88-4 methyl iodide 
• 4931-66-2 methyl (S)-pyroglutamate 

Downstream Products

• 1448345-68-3 C₂₄H₂₃ClF₃N₃O₃ 
• 89531-41-9 1-Methyl-5-hydroxymethyl-pyrrolidinon-(2) 
• 129896-88-4 2(S)-<(tert-butyloxycarbonyl)amino>-3-cyclohexyl-1(S)-hydroxy-1-(1-methyl-5(S)-ethenyl-2-oxopyrrolidin-3(S)-yl)propane 
• 122663-18-7 1-methyl-5(S)-vinyl-2-pyrrolidinone 
• 129896-90-8 2(S)-<(tert-butyloxycarbonyl)amino>-3-cyclohexyl-1(S)-hydroxy-1-(1-methyl-5(S)-<(benzyloxy)methyl>-2-oxopyrrolidin-3(S)-yl)propane 
• 129896-89-5 2(S)-<(tert-butyloxycarbonyl)amino>-3-cyclohexyl-1(S)-hydroxy-1-(1-methyl-5(S)-(methoxymethyl)-2-oxopyrrolidin-3(S)-yl)propane 
• 122663-21-2 5(S)-<(benzyloxy)methyl>-1-methyl-2-pyrrolidinone 
• 52574-06-8 (2S)-1-methyl-5-oxopyrrolidine-2-carboxylic acid 

Relevant academic research and scientific papers

SPIROCYCLIC TETRAHYDROQUINAZOLINES

Provided are compounds represented by Formula I, wherein R3, A, A1, A2, A3, E, E1, E2, L, Q, Z, and (aa) are as defined in the specification, and the pharmaceutically acceptable salts and solvates thereof. Compounds of Formula (I) are KRAS inhibitors and are thus useful to treat cancer and other diseases.

Spirocyclic tetrahydroquinazolines

The invention discloses spirocyclic tetrahydroquinazolines , and particularly provide compounds represented by Formula I shown in the specification, and pharmaceutically acceptable salts and solvates thereof. In the formula, R3, A, A1, A2, A3, E, E1, E2, L, Q, Z and a structure shown in the specification are as defined in the specification,. The compounds of formula I are KRAS inhibitors and are therefore useful in the treatment of cancer and other diseases.

Oxidative damage of proline residues by nitrate radicals (NO3): A kinetic and product study

Tertiary amides, such as in N-acylated proline or N-methyl glycine residues, react rapidly with nitrate radicals (NO3) with absolute rate coefficients in the range of 4-7 × 108 M-1 s-1 in acetonitrile. The major pathway proceeds through oxidative electron transfer (ET) at nitrogen, whereas hydrogen abstraction is only a minor contributor under these conditions. However, steric hindrance at the amide, for example by alkyl side chains at the α-carbon, lowers the rate coefficient by up to 75%, indicating that NO3-induced oxidation of amide bonds proceeds through initial formation of a charge transfer complex. Furthermore, the rate of oxidative damage of proline and N-methyl glycine is significantly influenced by its position in a peptide. Thus, neighbouring peptide bonds, particularly in the N-direction, reduce the electron density at the tertiary amide, which slows down the rate of ET by up to one order of magnitude. The results from these model studies suggest that the susceptibility of proline residues in peptides to radical-induced oxidative damage should be considerably reduced, compared with the single amino acid.

A Methyl Scan of the Pyrrolidinium Ring of Nicotine Reveals Significant Differences in Its Interactions with a7 and a4b2 Nicotinic Acetylcholine Receptors

The two major nicotinic acetylcholine receptors (nAChRs) in the brain are the a4b2 and a7 subtypes. A "methyl scan" of the pyrrolidinium ring was used to detect differences in nicotine's interactions with these two receptors. Each methylnicotine was investigated using voltage-clamp and radioligand binding techniques. Methylation at each ring carbon elicited unique changes in nicotine's receptor interactions. Replacing the 19-N-methyl with an ethyl group or adding a second 19-N-methyl group significantly reduced interaction with a4b2 but not a7 receptors. The 29-methylation uniquely enhanced binding and agonist potency at a7 receptors. Although 39- A nd 59-trans-methylations were much better tolerated by a7 receptors than a4b2 receptors, 49-methylation decreased potency and efficacy at a7 receptors much more than at a4b2 receptors. Whereas cis-59-methylnicotine lacked agonist activity and displayed a low affinity at both receptors, trans-59-methylnicotine retained considerable a7 receptor activity. Differences between the two 59-methylated analogs of the potent pyridyl oxymethylene-bridged nicotine analog A84543 were consistent with what was found for the 59-methylnicotines. Computer docking of the methylnicotines to the Lymnaea acetylcholine binding protein crystal structure containing two persistent waters predicted most of the changes in receptor affinity that were observed with methylation, particularly the lower affinities of the cis-methylnicotines. The much smaller effects of 19-, 39-, and 59-methylations and the greater effects of 29- A nd 49-methylations on nicotine a7 nAChR interaction might be exploited for the design of new drugs based on the nicotine scaffold.

THERAPEUTICALLY ACTIVE COMPOUNDS AND USE THEREOF

Provided are therapeutically active compounds and the use in manufacture of medicaments for treating a cancer characterized by the presence of a mutant allele of IDH1.

THERAPEUTICALLY ACTIVE COMPOUNDS AND THEIR METHODS OF USE

Provided are methods of treating a cancer characterized by the presence of a mutant allele of IDH1/2 comprising administering to a subject in need thereof a compound described here.

THERAPEUTICALLY ACTIVE COMPOUNDS AND THEIR METHODS OF USE

Provided are methods of treating a cancer characterized by the presence of a mutant allele of IDH1/2 comprising administering to a subject in need thereof a compound described here.

NICOTINE COMPOUNDS AND ANALOGS THEREOF, SYNTHETIC METHODS OF MAKING COMPOUNDS, AND METHODS OF USE

Embodiments of the present disclosure provide for compounds such as those shown in FIG. 1.1 (compounds A, B, C, and D), 2'substituted nicotine compounds, azetidine compounds, ether linked nicotine compounds (FIG. 1.2, compounds E, F, G, and H), methods of synthesis of the compounds, methods of treatment of a condition using compounds A, B, C, D, 2'substituted nicotine compounds, azetidine compounds, or ether linked nicotine compounds, methods of selectively stimulating alpha7 nAChR and/or alpha4beta2 receptors, and the like.

NOVEL COMPOUNDS AS CANNABINOID RECEPTOR LIGANDS

Disclosed herein are compounds of formula (I) wherein R1, R2, R3, R25a, R26a, X, and n are as defined in the specification. Pharmaceutical compositions comprising such compounds, and methods of treating conditions and disorders using such compounds and pharmaceutical compositions are also described

Method of preparing enantiomerically-pure 3-methyl-5-(1-alkyl-2(s)-pyrrolidinyl)isoxazoles

A novel process for preparing enantiomerically-pure 3-methyl-5-(1-(C1 -C3 -alkyl)-2-pyrrolidinyl)isoxazole in high yield, wherein a protected 2-oxo-pyrrolidine starting material is reacted with a suitable organic anion and a resulting beta-keto oxime intermediate is cyclized and dehydrated.