(-)-2,3-Dibenzoyl-L-tartaric acid - CAS 22333-70-6
Category:
Main Product
Product Name:
(-)-2,3-Dibenzoyl-L-tartaric acid
Catalog Number:
22333-70-6
Synonyms:
(-)-2,3-Dibenzoyl-L-tartaric acid; Dibenzoyltartaric acid
CAS Number:
22333-70-6
Molecular Weight:
358.30
Molecular Formula:
C18H14O8
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
C1=CC=C(C=C1)C(=O)OC(C(C(=O)O)OC(=O)C2=CC=CC=C2)C(=O)O
InChI:
InChI=1S/C18H14O8/c19-15(20)13(25-17(23)11-7-3-1-4-8-11)14(16(21)22)26-18(24)12-9-5-2-6-10-12/h1-10,13-14H,(H,19,20)(H,21,22)/t13-,14-/m1/s1
InChIKey:
YONLFQNRGZXBBF-ZIAGYGMSSA-N
Chemical Structure
CAS 22333-70-6 (-)-2,3-Dibenzoyl-L-tartaric acid

Reference Reading


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Huang CJ1, Lee CL2, Yang SH3, Chien CC4, Huang CC5, Yang RN6, Chang CC7. Biochim Biophys Acta. 2016 Apr 13. pii: S0925-4439(16)30081-3. doi: 10.1016/j.bbadis.2016.04.010. [Epub ahead of print]
Colorectal cancer (CRC) is one of the most common life-threatening malignances worldwide. CRC relapse markedly decreases the 5-year survival of patients following surgery. Aberrant expression of genes involved in pathways regulating the cell cycle, cell proliferation, or cell death are frequently reported in CRC tumorigenesis. We hypothesized that genes involved in CRC relapse might serve as prognostic indicators. We first evaluated the significance of gene sequences in the feces of patients with CRC relapse by consulting a public database. Tumorigenesis of target tissues was tested through tumor cell growth, cell cycle regulation, and chemotherapeutic efficacy. We found a highly significant correlation between CRC relapse and growth arrest-specific 2 (GAS2) gene expression. Based on cell models, the overexpressed GAS2 was associated with cellular growth rate, cell cycle regulation, and with chemotherapeutic sensitivity. Cell division was impaired by treating cells with 2-[4-(7-chloro-2-quinoxalinyloxy)phenoxy]-propionic acid (XK469), even when the cells were overexpressing GAS2.
2.Crosstalk between liver antioxidant and the endocannabinoid systems after chronic administration of the FAAH inhibitor, URB597, to hypertensive rats.
Biernacki M1, Łuczaj W1, Gęgotek A1, Toczek M2, Bielawska K1, Skrzydlewska E3. Toxicol Appl Pharmacol. 2016 Apr 13. pii: S0041-008X(16)30076-X. doi: 10.1016/j.taap.2016.04.006. [Epub ahead of print]
Hypertension is accompanied by perturbations to the endocannabinoid and antioxidant systems. Thus, potential pharmacological treatments for hypertension should be examined as modulators of these two metabolic systems. The aim of this study was to evaluate the effects of chronic administration of the fatty acid amide hydrolase (FAAH) inhibitor [3-(3-carbamoylphenyl)phenyl]N-cyclohexylcarbamate (URB597) on the endocannabinoid system and on the redox balance in the livers of DOCA-salt hypertensive rats. Hypertension caused an increase in the levels of endocannabinoids [anandamide (AEA), 2-arachidonoyl-glycerol (2-AG) and N-arachidonoyl-dopamine (NADA)] and CB1 receptor and the activities of FAAH and monoacylglycerol lipase (MAGL). These effects were accompanied by an increase in the level of reactive oxygen species (ROS), a decrease in antioxidant activity/level, enhanced expression of transcription factor Nrf2 and changes to Nrf2 activators and inhibitors.
3.Design and synthesis of some novel 4-Chloro-N-(4-(1-(2-(2-cyanoacetyl)hydrazono)ethyl)phenyl) benzenesulfonamide derivatives as anticancer and radiosensitizing agents.
Ghorab MM1, Ragab FA2, Heiba HI3, Soliman AM3. Eur J Med Chem. 2016 Apr 6;117:8-18. doi: 10.1016/j.ejmech.2016.04.009. [Epub ahead of print]
A novel series of sulfonamide derivatives 4-21 have been synthesized starting from the strategic starting material (E)-4-Chloro-N-(4-(1-(2-(2-cyanoacetyl)hydrazono)ethyl)phenyl) benzenesulfonamide 4. Two series of hydrazone 5-9, and pyridone 10-21 derivatives bearing a sulfonamide moiety were obtained. All the newly synthesized compounds were evaluated for their in vitro cytotoxic activity against human liver cancer cell line (HepG2). Compounds 4-6, 8, 9, 10-14 and 16-18 showed higher activity compared to doxorubicin as a positive control. The radiosensitizing ability of the most promising compounds 4, 10 and 12 was studied which showed an increase in the cell killing effect of γ-radiation after combination with these derivatives. The molecular design was performed to predict the binding mode of the most promising compounds 4, 10 and 12 with the active site of hCA IX, that showed appropriate fitting with the relevant amino acids in the binding pocket on the basis of standard bond lengths, angles, S score and E conformation data.
4.Parathyroid hormone levels and high-residual platelet reactivity in patients receiving dual antiplatelet therapy with acetylsalicylic acid and clopidogrel or ticagrelor.
Verdoia M1, Pergolini P2, Rolla R2, Nardin M1, Barbieri L1, Schaffer A1, Bellomo G2, Marino P1, Suryapranata H1, De Luca G1; Novara Atherosclerosis Study Group (NAS). Cardiovasc Ther. 2016 Apr 17. doi: 10.1111/1755-5922.12188. [Epub ahead of print]
BACKGROUND: High on treatment platelet reactivity still represents a challenging issue, potentially vanishing the benefits of dual antiplatelet treatment in patients with coronary artery disease. However, very few is known on the determinants of suboptimal response to antiplatelet agents. Recent interests have emerged on the potential protrombotic effect of parathyroid hormone (PTH). Therefore, the aim of the present study was to assess the impact of parathyroid hormone (PTH) on platelet reactivity in patients receiving DAPT after an acute coronary syndrome or PCI.