64370-53-2

Upstream product

• 147-71-7 D-tartaric acid 
• 908093-98-1 diazodiphenylmethane 
• 5350-57-2 benzophenone hydrazone 

Downstream Products

• 222320-55-0 bis(diphenylmethyl) bis-D-tartrate 
• 222320-57-2 bis(diphenylmethyl) dicaffeoyl-D-tartrate 
• 1427216-38-3 C₄₈H₃₈O₈ 
• 1427216-40-7 C₅₂H₄₂O₁₄ 
• 1427216-43-0 C₅₄H₄₆O₁₆ 

Relevant academic research and scientific papers

Synthesis of tartaric acid analogues of FR258900 and their evaluation as glycogen phosphorylase inhibitors

Di-O-cinnamoylated, -p-coumaroylated, and -feruloylated d-, l- and meso-tartaric acids were synthesized as analogues of the natural product FR258900, a glycogen phosphorylase (GP) inhibitor with in vivo antihyperglycaemic activity. The new compounds inhib

Novel HIV integrase inhibitors and HIV therapy based on drug combinations including integrase inhibitors

The present invention includes a group of novel compounds that are demonstrated to potently and selectively inhibit HIV integrase (IN) activity in vitro and to potently inhibit HIV replication in live, cultured cells at non-toxic concentrations. The novel

Structure-activity relationships: Analogues of the dicaffeoylquinic and dicaffeoyltartaric acids as potent inhibitors of human immunodeficiency virus type 1 integrase and replication

The dicaffeoylquinic acids (DCQAs) and dicaffeoyltartaric acids (DCTAs) are potent and selective inhibitors of human immunodeficiency virus type 1 (HIV-1) integrase. They also inhibit HIV-1 replication at nontoxic concentrations. Since integrase is an excellent target for anti-HIV therapy, structure-activity relationships were employed to synthesize compounds with: (1) improved potency against HIV-1 integrase, (2) improved anti-HIV effect in tissue culture, and (3) increased selectivity as indicated by low cellular toxicity. Thirty-four analogues of the DCTAs and DCQAs were synthesized and tested for cell toxicity, anti-HIV activity, and inhibition of HIV-1 integrase. Seventeen of the 34 analogues had potent activity against HIV-1 integrase ranging from 0.07 to > 10 μM. Seventeen analogues that were synthesized or purchased had no inhibitory activity against integrase at concentrations of 25 μM. Of the biologically active analogues, 7 of the 17 inhibited HIV replication at nontoxic concentrations. The most potent compounds were D-chicoric acid, meso-chicoric acid, bis(3,4- dihydroxydihydrocinnamoyl)-L-tartaric acid, digalloyl-L-tartaric acid, bis(3,4-dihydroxybenzoyl)-L-tartaric acid, dicaffeoylglyceric acid, and bis(3,4-dihydroxyphenylacetyl)-L-tartaric acid. Anti-HIV activity of the active compounds in tissue culture ranged from 35 to 0.66 μM. Structure- activity relationships demonstrated that biscatechol moieties were absolutely required for inhibition of integrase, while at least one free carboxyl group was required for anti-HIV activity. These data demonstrate that analogues of the DCTAs and the DCQAs can be synthesized which have improved activity against HIV integrase.