147291-52-9

Upstream product

• 55737-62-7 methyl 4-(chlorocarbonyl)-2-nitrobenzoate 
• 75-65-0 tert-butyl alcohol 
• 35092-89-8 4-(methoxycarbonyl)-3-nitrobenzoic acid 
• 115-11-7 isobutene 
• 5292-45-5 dimethyl 2-nitroterephthalate 

Downstream Products

• 863905-89-9 3-methoxycarbonylmethoxy-6-(5-methyl-1-phenyl-1H-pyrazol-3-ylcarbamoyl)benzo[b]thiophene-2-carboxylic acid methyl ester 
• 1374777-62-4 2-[N-(3-chlorobenzo[b]thiophene-2-carbonyl)-N-methylamino]-4-(4-chlorophenylcarbamoyl)benzoic acid 
• 1374779-35-7 C₂₅H₁₈Cl₂N₂O₄S 
• 1374779-34-6 C₁₉H₁₄ClNO₅S 
• 1374779-33-5 C₂₃H₂₂ClNO₅S 
• 1374779-32-4 C₂₂H₂₀ClNO₅S 
• 147291-57-4 {8-[4-(tert-butoxycarbonylamino-imino-methyl)-phenylcarbamoyl]-5-oxo-4-phenethyl-2,3,4,5-tetrahydro-1H-benzo[e][1,4]diazepin-2-yl}-acetic acid methyl ester 
• 223587-41-5 (Z)-methyl 4--N-(2-phenylethyl)amino>-2-butenoate 
• 147291-55-2 methyl (R,S)-8-carboxy-1,2,4,5-tetrahydro-5-oxo-4-(2-phenylethyl)-5H-1,4-benzodiazepine-2-acetate 
• 147291-53-0 5,N-bis(tert-butyloxycarbonyl)-2-(methoxycarbonyl)aniline 
• 849793-90-4 4-(tert-butyl) 1-methyl 2-aminoterephthalate 

Relevant academic research and scientific papers

MODIFIED PROTEINS AND PROTEIN DEGRADERS

Provided herein are compounds, pharmaceutical compositions, and methods for binding or degrading target proteins. Further provided herein are compounds having a DNA damage-binding protein 1 (DDB1) binding moiety. Some such embodiments include a linker. Some such embodiments include a target protein binding moiety. Further provided herein are ligand-DDB1 complexes. Further provided herein are in vivo modified DDB1 proteins.

NEUROTRYPSIN INHIBITORS

The invention relates to acylamino-phthalic acid amides and related compounds of formula (I) wherein A is -CONR3R4,-NR5COR6, -NHR7, -OR8, -mR9, -CH2NRI0R11, -(CH2)2-R12, -CH=CH-R12, -C=C-R12, optionally substituted phenyl, optionally substituted thiophenyl, or optionally substituted 1,2,3-triazol-4-yl, W is hydrogen, hydroxy or carboxymethoxy, Y is carboxy, methoxycarbonyl or 2H-tetrazol-5-yl, and the various substituents R have the meanings indicated in the description. These compounds are useful for the treatment and/or prophylaxis of skeletal muscle atrophy, schizophrenia and Alzheimer?s disease, and as cognitive enhancers.

PTP1b inhibitors

This invention relates to modulating (e.g., inhibiting) protein tyrosine phosphatase 1B (PTP1B).

Bicyclic and tricyclic thiophenes as protein tyrosine phosphatase 1B inhibitors

A novel pyridothiophene inhibitor of PTP1B was discovered by rational screening of phosphotyrosine mimics at high micromolar concentrations. The potency of this lead compound has been improved significantly by medicinal chemistry guided by X-ray crystallo

Inhibitors of protein tyrosine phosphatase 1B

Protein tyrosine phosphatases (PTPases) such as PTP1B can play a role in regulating a wide variety of cellular responses such as insulin signaling. Substituted bicyclic fused-thiophene compounds can inhibit PTP1B and thereby induce greater insulin sensitivity. Accordingly, PTP1B inhibition can provide an alternate treatment for PTPase-mediated disorders such as diabetes.

Conformational preferences in a benzodiazepine series of potent nonpeptide fibrinogen receptor antagonists

Previously, we reported the direct design of highly potent nonpeptide 3- oxo-1,4-benzodiazepine fibrinogen receptor antagonists from a constrained, RGD-containing cyclic semipeptide. The critical features incorporated into the design of these nonpeptides were the exocyclic amide at the 8-position which overlaid the Arg carbonyl, the phenyl ring which maintained an extended Gly conformation, and the diazepine ring which mimicked the γ-turn at Asp. In this paper, we investigate conformational preferences of the 8-substituted benzodiazepine analogues by examining structural modifications to both the exocyclic amide and the seven-membered diazepine ring and by studying the conformation of the benzodiazepine ring using molecular modeling, X-ray crystallography, and NMR. We found that the directionality of the amide at the 8-position had little effect on activity and the (E)-olefin analogue retained significant potency, indicating that the trans orientation of the amide, and not the carbonyl or NH groups, made the largest contribution to the observed activity. For the diazepine ring, with the exception of the closely analogous 3-oxo-2-benzazepine ring system described previously, all of the modifications led to a significant reduction in activity compared to the potent 3-oxo-1,4-benzodiazepine parent ring system, implicating this particular type of ring system as a desirable structural feature for high potency. Energy minimizations of a number of the modified analogues revealed that none could adopt the same low-energy conformation as the one shared by the active (S)-isomer of the 3-oxo-1,4-benzodiazepines and 3-oxo-2- benzazepines. The overall data suggest that the features contributing to the observed high potency in this series are the orientation of the 3-4 amide and the conformational constraint imposed by the seven-membered ring, both of which position the key acidic and basic groups in the proper spatial relationship.

Bicyclic fibrinogen antagonists

This invention relates to compounds of the formula: STR1 wherein A1 to A5 form an accessible substituted seven-membered ring, which may be saturated or unsaturated, optionally containing up to two heteroatoms chosen from the group of O, S and N wherein S and N may be optionally oxidized; D1 to D4 form an accessible substituted six membered ring, optionally containing up to two nitrogen atoms; R is at least one substituent chosen from the group of R7, or Q--C1-4 alkyl, Q--C2-4 alkenyl, Q--C2-4 alkynyl, preferably substituted by an acidic function; R* is H, Q--C1-6 alkyl, Q--C1-6 oxoalkyl, Q--C2-6 alkenyl or Q--C2-4 alkynyl, C3-6 cycloalkyl, Ar or Het, optionally substituted by one or more substitutents; and R6 is preferably a substituent containing a basic nitrogen moiety; or a pharmaceutically acceptable salt thereof, which are effective for inhibiting platelet aggregation, pharmaceutical compositions for effecting such activity, and a method for inhibiting platelet aggregation.