28845-94-5Relevant articles and documents
-
Pfeffer,P.E. et al.
, p. 1256 - 1258 (1972)
-
Preparative Enantioseparation of β-Substituted-2-Phenylpropionic Acids by Countercurrent Chromatography with Substituted β-Cyclodextrin as Chiral Selectors
Tong, Shengqiang,Zhang, Hu,Cheng, Dongping
, p. 795 - 801 (2015)
Preparative enantioseparation of four β-substituted-2-phenylpropionic acids was performed by countercurrent chromatography with substituted β-cyclodextrin as chiral selectors. The two-phase solvent system was composed of n-hexane-ethyl acetate-0.10olL-1 of phosphate buffer solution at pH2.67 containing 0.10olL-1 of hydroxypropyl-β-cyclodextrin (HP-β-CD) or sulfobutylether-β-cyclodextrin (SBE-β-CD). The influence factors, including the type of substituted β-cyclodextrin, composition of organic phase, concentration of chiral selector, pH value of the aqueous phase, and equilibrium temperature were optimized by enantioselective liquid-liquid extraction. Under the optimum separation conditions, 100g of 2-phenylbutyric acid, 100g of tropic acid, and 50g of 2,3-diphenylpropionic acid were successfully enantioseparated by high-speed countercurrent chromatography, and the recovery of the (±)-enantiomers was in the range of 90-91% for (±)-2-phenylbutyric acid, 91-92% for (±)-tropic acid, 85-87% for (±)-2,3-diphenylpropionic acid with purity of over 97%, 96%, and 98%, respectively. The formation of 1:1 stoichiometric inclusion complex of β-substituted-2-phenylpropionic acids with HP-β-CD was determined by UV spectrophotometry and the inclusion constants were calculated by a modified Benesi-Hildebrand equation. The results showed that different enantioselectivities among different racemates were mainly caused by different enantiorecognition between each enantiomer and HP-β-CD, while it might be partially caused by different inclusion capacity between racemic solutes and HP-β-CD.
-
Gibson,Youngken
, p. 854,855 (1967)
-
The isolation of 6 hydroxyhyocyamine from a Duboisia hybrid
Griffin
, p. 97 - 97 (1975)
-
Synthesis method of 3-hydroxy-2-phenylpropionic acid
-
Paragraph 0024; 0027-0029; 0030; 0032-0035; 0036; 0039-0041, (2019/12/25)
The invention discloses a synthetic method of 3-hydroxyl-2-phenylpropionic acid. The method comprises the following steps: mixing dimethyl sulfoxide, paraformaldehyde, potassium carbonate powder and methyl phenylacetate, heating to 85-95 DEG C, carrying out gas phase monitoring reaction, and cooling to room temperature when the GC content of the product methyl tropine is more than or equal to 70%;adjusting the pH value to be neutral, and performing reduced pressure distillation for desolvation; then adding methanol into the desolventized mixture, dropwise adding a sodium hydroxide solution, and reacting to obtain a mixed solution containing sodium tropine salt; adjusting the pH value of the mixed solution to 2-3, and completely reacting to obtain a crude product; and finally, recrystallizing the crude product sequentially by using methylbenzene of which the ratio of m product to m methylbenzene is 1: (4-6), methylbenzene/water of which the ratio of m product to m methylbenzene to m water is 1: (1-2): (4-6), and water of which the ratio of m product to m water is 1: (4-6) to obtain a pure product of 3-hydroxyl-2-phenylpropionic acid. According to the method, GC is adopted to monitor the reaction, control points are judged quickly and accurately, purification of methyl tropinate is not needed, operation procedures are reduced, and production cost is reduced. According to the method, the purity of the prepared 3-hydroxyl-2-phenylpropionic acid reaches 99% or above while the yield is ensured to reach 76.5% or above.
SUBSTITUTED PYRAZOLO[1,5-A]PYRIDINE COMPOUNDS AS RET KINASE INHIBITORS
-
Paragraph 00742, (2017/02/09)
Provided herein are compounds of the General Formula I: and stereoisomers and pharmaceutically acceptable salts or solvates thereof, in which A, B, D, E, X1, X2, X3 and X4 have the meanings given in the specification, which are inhibitors of RET kinase and are useful in the treatment and prevention of diseases which can be treated with a RET kinase inhibitor, including diseases or disorders mediated by a RET kinase.