75351-36-9

Upstream product

• 20585-18-6 methyl 4,6-dideoxy-α-D-glucopyranoside 
• 98-59-9 p-toluenesulfonyl chloride 
• 6290-03-5 (R)-butane-1,3-diol 
• 1312789-89-1 (3R)-3-acetoxybutyl 4-methylbenzenesulfonate 

Downstream Products

• 109613-35-6 (R)-3-[(tert-butyldimethylsilyl)oxy]butane-1-para-toluene sulfonate 
• 946133-90-0 (3R)-1-p-toluenesulfonyloxy-3-triethylsilyloxy-butane 
• 1215219-59-2 (R)-1-(phenylselanyl)-3-butanol 
• 1215219-60-5 (R)-1-(phenyltellanyl)-3-butanol 
• 134641-08-0 (R)-4-(phenylthio)-2-butanol 
• 610318-98-4 C₂₆H₂₇ClF₃NO 
• 1193686-56-4 C₁₃H₁₈O₄ 
• 1294453-54-5 (2R)-4-(4-bromo-3,5-dimethylphenoxy)butan-2-ol 
• 1208313-97-6 (R)-3-hydroxybutyrate (R)-1,3-butanediol monoester 
• 58917-25-2 (R)-5-methyl-2-oxotetrahydrofuran 
• 1310533-97-1 (R)-1-(3-hydroxybutyl)-3-mesityl-1H-imidazol-3-ium 4-methylbenzenesulfonate 
• 81244-76-0 (R)-(-)-2-Methyloxetane 

Relevant academic research and scientific papers

Preparation method of (R)-3-hydroxybutyryl-(R)-3-hydroxybutyrate

The invention discloses a preparation method of (R)-3-hydroxybutyryl-(R)-3-hydroxybutyrate. The preparation method comprises the following steps: (1) subjecting a compound (III) to reacting with paratoluensulfonyl chloride in a first solvent in the presence of alkali to obtain a compound (II); and (2) subjecting the compound (II) to reacting with (R)-3-hydroxybutyrate in a second solvent, or subjecting the compound (II) to reacting with (R)-3-hydroxybutyric acid in the presence of alkali. According to the invention, a route is simple, protection/deprotection reaction is avoided, the product can be obtained through two-step reaction from easily available raw materials, total yield is larger than or equal to 70%, and the purity of the product is larger than or equal to 95% without refining; and the method has the advantages of mild process conditions, no need for special equipment, low cost and suitability for industrial amplification, and related reagents and solvents are cheap and easy to obtain.

Achieving in Vivo Target Depletion through the Discovery and Optimization of Benzimidazolone BCL6 Degraders

Deregulation of the transcriptional repressor BCL6 enables tumorigenesis of germinal center B-cells, and hence BCL6 has been proposed as a therapeutic target for the treatment of diffuse large B-cell lymphoma (DLBCL). Herein we report the discovery of a series of benzimidazolone inhibitors of the protein-protein interaction between BCL6 and its co-repressors. A subset of these inhibitors were found to cause rapid degradation of BCL6, and optimization of pharmacokinetic properties led to the discovery of 5-((5-chloro-2-((3R,5S)-4,4-difluoro-3,5-dimethylpiperidin-1-yl)pyrimidin-4-yl)amino)-3-(3-hydroxy-3-methylbutyl)-1-methyl-1,3-dihydro-2H-benzo[d]imidazol-2-one (CCT369260), which reduces BCL6 levels in a lymphoma xenograft mouse model following oral dosing.

SUBSTITUTED BENZIMIDAZOLONES AS ANTI-CANCER AGENTS

The present invention relates to compounds of Formula I that function as inhibitors of BCL6 (B-cell lymphoma 6) activity: Formula (I) wherein X, R1, R2, and R3 are each as defined herein. The present invention also relates to processes for the preparation of these compounds, to pharmaceutical compositions comprising them, and to their use in the treatment of proliferative disorders, such as cancer, as well as other diseases or conditions in which BCL6activity is implicated.

Heterocyclic compound as TRK inhibitor

The present invention relates to a compounds, a pharmaceutical compositions containing the compound, preparation methods of the compound and the pharmaceutical composition, and uses of the compound and the pharmaceutical composition as TRK inhibitors, wherein the compound is a compound represented by a formula I, or a pharmaceutically acceptable salt, a prodrug, a solvent compound, a polymorph, anisomer and a stable isotope derivative thereof. The invention further relates to uses of the compound in treatment or prevention of TRK-mediated related diseases such as tumors, and a method for treating the diseases by using the compound.

2 Tyrosine kinase mediated signal transduction inhibitors

Disclosed herein are compounds of Formula (), and pharmaceutically acceptable salts thereof, wherein R, R, R, R, R, X, X, X, X, X, and n are as defined herein, pharmaceutical compositions comprising same, and methods of preparation and use.

NOVEL SUBSTITUTED XANTHINE DERIVATIVES

The present invention relates to substituted xanthine derivatives, pharmaceutical compositions containing them and their use in therapy, particularly in the treatment of conditions having an association with TRPC5 containing ion channels.

BENZIMIDAZOLONE DERIVED INHIBITORS OF BCL6

The present invention relates to compounds of Formula I that function as inhibitors of BCL6 (B-cell lymphoma 6) activity: wherein X1, X2, R1, R2 and R3 are each as defined herein. The present invention also relates to processes for the preparation of these compounds, to pharmaceutical compositions comprising them, and to their use in the treatment of proliferative disorders, such as cancer, as well as other diseases or conditions in which BCL6 activity is implicated.

Regio- and Enantioselective Sequential Dehalogenation of rac-1,3-Dibromobutane by Haloalkane Dehalogenase LinB

The hydrolytic dehalogenation of rac-1,3-dibromobutane catalyzed by the haloalkane dehalogenase LinB from Sphingobium japonicum UT26 proceeds in a sequential fashion: initial formation of intermediate haloalcohols followed by a second hydrolytic step to produce the final diol. Detailed investigation of the course of the reaction revealed favored nucleophilic displacement of the sec-halogen in the first hydrolytic event with pronounced R enantioselectivity. The second hydrolysis step proceeded with a regioselectivity switch at the primary position, with preference for the S enantiomer. Because of complex competition between all eight possible reactions, intermediate haloalcohols formed with moderate to good ee ((S)-4-bromobutan-2-ol: up to 87 %). Similarly, (S)-butane-1,3-diol was formed at a maximum ee of 35 % before full hydrolysis furnished the racemic diol product.

Isolation, Structure Elucidation, and (Bio)Synthesis of Haprolid, a Cell-Type-Specific Myxobacterial Cytotoxin

Myxobacteria are well-established sources for novel natural products exhibiting intriguing bioactivities. We here report on haprolid (1) isolated from Byssovorax cruenta Har1. The compound exhibits an unprecedented macrolactone comprising four modified amino acids and a polyketide fragment. As configurational assignment proved difficult, a bioinformatic analysis of the biosynthetic gene cluster was chosen to predict the configuration of each stereocenter. In-depth analysis of the corresponding biosynthetic proteins established a hybrid polyketide synthase/nonribosomal peptide synthetase origin of haprolid and allowed for stereochemical assignments. A subsequent total synthesis yielded haprolid and corroborated all predictions made. Intriguingly, haprolid showed cytotoxicity against several cell lines in the nanomolar range whereas other cells were almost unaffected by treatment with the compound.

METHOD FOR PRODUCING 3-BUTENE-2-OL

PROBLEM TO BE SOLVED: To provide a method for efficiently producing racemic 3-butene-2-ol having an (S)- or (R)-configuration. SOLUTION: There is provided a method for producing racemic 3-butene-2-ol, wherein an ammonium salt compound represented by the following general formula (1) (wherein, R1, R2 or R3 represents an alkyl group, an aryl group or an aralkyl group; X- represents OH-, HCO3-, CO32-, R4O-, R5CO2-, R6SO3- (R4, R5 or R6 represents an alkyl group, an aryl group or an aralkyl group) and a halide ion; n represents 0.5 when X- is CO32- and n represents 1 when X- is other than CO32-; the carbon atom marked with * is an asymmetric carbon atom) is subjected to Hofmann elimination. COPYRIGHT: (C)2016,JPOandINPIT