Detail of "635-51-8"

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CAS Number:
635-51-8
Name:
Butanedioicacid, 2-phenyl-
Superlist Name:
DL-Phenylsuccinic acid
Molecular Structure:
Formula:
C₁₀H₁₀O₄
Molecular Weight:
194.184
Deleted CAS:
10424-29-0
Synonyms:
Butanedioicacid, phenyl- (9CI);Succinic acid, phenyl- (6CI,7CI,8CI);(RS)-Phenylsuccinicacid;2-Phenylbutanedioic acid;2-Phenylsuccinic acid;NSC 11342;NSC 16635;Phenylsuccinic acid;a-Phenylsuccinicacid;
EINECS:
211-238-1
Density:
1.336 g/cm³
Melting Point:
166-168 °C(lit.)
Boiling Point:
307.8 °C at 760 mmHg
Flash Point:
154.2 °C
Solubility:
Very soluble in water
Appearance:
light beige powder
Hazard Symbols:
Xi
Risk Codes:
36/37/38
Safety:
22-24/25-37/39-26 Details

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Reference

Effect of phenylsuccinate on potassium- and ischemia-induced release of glutamate in rat hippocampus monitored by microdialysis: Effect of phenylsuccinate on potassium- and ischemia-induced release of glutamate in rat hippocampus monitored by microdialysis. Christensen, Thomas; Bruhn, Torben; Diemer, Nils H.; Schousboe, Arne (Inst. Neuropathol., Univ. Copenhagen, Copenhagen DK-2100, Den.). Neurosci. Lett., Volume Date 1992, 134(1), 71-4 (English) 1991. CODEN: NELED5. ISSN: 0304-3940. DOCUMENT TYPE: Journal CA Section: 13 (Mammalian Biochemistry) Section cross-reference(s): 2, 14 The extracellular concn. of glutamate in rat hippocampus during physiol. conditions, elevated extracellular K+ and global ischemia was followed by microdialysis and subsequent detn. of glutamate by HPLC. The effect of phenylsuccinate, an inhibitor of the mitochondrial dicarboxylate carrier, was studied. It was found that while phenylsuccinate had no effect on the extracellular glutamate concn. during perfusion under physiol. and ischemic conditions, the potassium-induced increase in the extracellular glutamate concn. 635-51-8 and 7440-09-7 which are cas registry numbers of chemicals are mentioned. was totally blocked by phenylsuccinate. Ischemia led to a pronounced glutamate overflow. The finding that phenylsuccinate could inhibit potassium-induced glutamate release into the extracellular space but not that induced by ischemia suggests that glutamate released under these conditions originates from different pools. Since glutamate released by a depolarizing concn. of potassium is likely to originate primarily from the transmitter pool, the ischemia-induced glutamate overflow may primarily be released from both the transmitter and the metabolic pool. This is compatible with the previous finding that phenylsuccinate specifically prevents biosynthesis of transmitter glutamate leaving the metabolic glutamate pool unaffected. .

Bond fixation in annulenes: Bond fixation in annulenes. 16. Synthesis of the 1,2-dimethyl-3-phenylcyclooctatetraene t 1,8-dimethyl-2-phenylcyclooctatetraene bond shift isomer pair. Probe of the relative size of a flanking phenyl substituent by means of racemization kinetics. Paquette, Leo A.; Gardlik, John M.; McCullough, Kevin J.; Samodral, Rodney; DeLucca, George; Ouellette, Robert J. (Evans Chem. Lab., Ohio State Univ., Columbus, OH 43210, USA). J. Am. Chem. Soc., 105(26), 7649-55 (English) 1983. CODEN: JACSAT. ISSN: 0002-7863. DOCUMENT TYPE: Journal CA Section: 22 (Physical Organic Chemistry) Two synthetic approaches to the cyclooctatetraene bond-shift isomers I t II were developed. The 1st began with a Ph-substituted starting material (HO2CCHPhCH2CO2H) and proceeded to introduce the 2 Me groups by desulfonylative ring contraction of a bicyclic a,a'-disubstituted sulfone. The 2nd had its origins in citraconic anhydride. Both pathways were dependent upon regioselective bromination-dehydrobromination of a bicyclo[4.2.0]octadiene to generate the cyclooctatetraene nucleus. Although I dominates over II in the equil. 87923-90-8 and 635-51-8 which are cas registry numbers of chemicals are mentioned., it is possible to sep. these bond-shift isomers by cycloaddn. with a triazolinedione. When recourse was made to the endo-bornyl-substituted dienophile, it was ultimately possible to obtain (-)-I and to det. its rate of racemization. The flanking Ph group in I causes significant rate retardation relative to the tri-Me deriv. This finding contrasts with the behavior of III, which racemizes more rapidly despite an interstitial Ph substituent. The source of these dissimilar effects was clarified by MM2 calcns., the details of which are presented. .

Detail of "635-51-8"

Butanedioicacid, 2-phenyl-

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CAS No.635-51-8 DL-Phenylsuccinic acid

CAS No.635-51-8 DL-Phenylsuccinic acid

CAS No.635-51-8 DL-Phenylsuccinic acid

CAS No.635-51-8 DL-Phenylsuccinic acid

Reference