50587-77-4

Upstream product

• 3378-72-1 N-tert-butylbenzylamine 
• 590-17-0 cyanomethyl bromide 
• 107-14-2 chloroacetonitrile 

Downstream Products

• 487065-49-6 (2S,3S,4R)-N-benzyl-N-tert-butyl-4,5-O-isopropylidene-2-amino-3,4,5-trihydroxyvaleronitrile 
• 847573-72-2 4-[[2-(N-benzyl-N-tert-butylamino)ethyl]amino]-6,7-methylenedioxyquinoline 
• 847573-89-1 12-[2-(benzyl-tert-butyl-amino)-ethyl]-2,3-dimethoxy-12H-8,10-dioxa-6,12-diaza-cyclopenta[b]chrysen-13-one 
• 847573-81-3 N-(6,7-methylenedioxyquinolin-4-yl)-N-[2-(N-benzyl-N-tert-butylamino)ethyl]-2-iodo-4,5-dimethoxybenzamide 
• 61694-29-9 N-[2-(N'-benzyl-N'-tert-butylamino)ethyl]-4-amino-5-chloro-2-methoxybenzamide 

Relevant academic research and scientific papers

ANTAGONISTS OF THE KAPPA OPIOID RECEPTOR

The present technology is directed to compounds, compositions, and methods related to non-morphinan-like kappa opioid receptor (KOR) antagonists. The technology is suited to treat addiction, diuresis, depression, post traumatic stress disorder, an eating

Potency enhancement of the κ-opioid receptor antagonist probe ML140 through sulfonamide constraint utilizing a tetrahydroisoquinoline motif

Optimization of the sulfonamide-based kappa opioid receptor (KOR) antagonist probe molecule ML140 through constraint of the sulfonamide nitrogen within a tetrahydroisoquinoline moiety afforded a marked increase in potency. This strategy, when combined wit

THERAPEUTIC AGENT FOR CEREBRAL INFARCTION

The invention provides a therapeutic drug for ischemic stroke. The therapeutic drug has the formula (I) wherein each symbol is as defined herein, or a pharmacologically acceptable salt thereof, or a solvate thereof, as an active ingredient.

5-(2-Aminoethyl)dibenzo[c,h][1,6]naphthyridin-6-ones: Variation of N-alkyl substituents modulates sensitivity to efflux transporters associated with multidrug resistance

5H-8,9-Dimethoxy-5-(2-N,N-dimethylaminoethyl)-2,3-methylenedioxydibenzo[c, h]-[1,6]naphthyridin-6-one (ARC-111) has potent TOP1-targeting activity and pronounced antitumor activity. Several analogues of ARC-111 were synthesized with NH2, N-alkyl, N,N-dialkyl, pyrrolidinyl, piperidinyl, and piperazinyl substituents at the 2-position of the 5-ethyl group. The relative TOP1-targeting activity and cytotoxicity of these structural analogues were assessed in RPMI8402 and P388 tumor cells and their camptothecin-resistant variants CPT-K5 and P388/CPT45, respectively. Potent TOP1-targeting activity was retained within a series of mono N-alkyl analogues that included NHCH 2CH3, NHCH(CH3)2, and NHC(CH 3)3. TOP1-targeting activity was diminished by the presence of a N-benzyl moiety. In a comparison of a series of N-alkyl-N-isopropyl analogues, activity decreased in the order CH3 > CH2CH3 > CH-(CH3)2. Cytotoxicity in RPMI8402 and P388 did correlate with TOP1-targeting activity. Cytotoxic activity was also determined in KB3-1 cells and its variants KB/V-1 and KBH5.0. As KB/V-1 cells overexpress MDR1 and KBH5.0 cells overexpress BCRP, decreased cytotoxicity in these cell lines relative to the parent cell line is indicative of compounds that are substrates for these efflux transporters. In view of their diminished cytotoxicity in KB/V-1 cells, it appears that the likely demethylated metabolites of ARC-111, i.e., where NH2 or NHCH3 replaces the N(CH3)2 at the 2-position of the 5-ethyl substituent, are substrates for MDR1. In contrast, no significant difference in cytotoxicity among these three cell lines was observed with other N-alkyl analogues, including NHC2H5, NHCH(CH 3)2, NHC(CH3)3, N(CH 3)2, N(CH2CH3)2, NCH 3(CH-(CH3)2), and either the pyrrolidinyl or the piperidinyl analogues. The 2-(piperazinyl) analogues were associated with diminished cytotoxicity in KB/V-1 cells, suggesting that the second basic amino substituent is associated with their recognition as substrates by MDR1. Comparative studies on the antitumor activity of ARC-111 and its N-demethylated derivatives (the NHCH3 and NH2 analogues) against SJ-BT45 medulloblastoma xenografts in seid mice revealed that the secondary amine metabolite is at least as active as ARC-111 in vivo, although the primary amine derivative was significantly less potent.

Diastereoselective aldolization of α-aminonitriles. Diastereoselective synthesis of β-amino alcohols and β,γ-diamino alcohols

Aldolization performed by addition of lithiated N-benzyl-N-tert-butylaminoacetonitrile to aldehydes provides diastereomerically pure anti-β-hydroxy-α-aminonitriles. They are transformed into syn,anti-protected β,γ-diamino alcohols by a two-step procedure, involving addition of a Grignard reagent and reduction. The cleavage of the N-tert-butyl group is achieved by a simple acidic treatment. The application of this methodology to chiral, nonracemic aldehydes is studied. Starting from D-isopropylideneglyceraldehyde, an anti, anti, syn, anti-(2R,3S,4S,5R,6R)-diaminotriol is prepared in acceptable yield and with a good level of diastereoselectivity.