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1 f the GABA(B) agonist, 3-aminopropyl-(methyl)phosphinic acid.
2 dary phosphine, and finally oxidation to the phosphinic acid.
3 ficient method for the synthesis of glycosyl phosphinic acids (21) from the corresponding C-phosphona
4 competitive antagonist 3-aminopropyl(methyl)phosphinic acid (3-APMPA) induced fluorescence changes i
5 l)ethyl]amino-2-hydroxypropyl](phenylme thyl)phosphinic acid] (a GABA(B) antagonist)-sensitive respon
6 el and practical approach to monosubstituted phosphinic acid (alkylphosphonous acid) derivatives from
8 hylene glutaric acid ester provided the aryl phosphinic acid analogue of p-aminobenzoyl glutamic acid
9 protecting groups, provided the target aryl phosphinic acid analogues of folic acid and related anti
10 r concentrations, both 3-aminopropyl(methyl)-phosphinic acid and GABA directly activated the A, G, S,
11 thesis of suitably protected p-aminophenyl H-phosphinic acids and esters from the corresponding para-
12 pon previous routes for the preparation of H-phosphinic acids and other organophosphorus compounds.
16 III)) cations with bis(2,4,4-trimethylpentyl)phosphinic acid, bis(2,4,4-trimethylpentyl)monothiophosp
17 ophenyl)-methyl]amino]propyl](diethoxymethyl)phosphinic acid blocked ACh-induced reduction in the evo
18 ic approaches, not only to prepare allylic H-phosphinic acids but also their esters via one-pot tande
24 ious PIII species derived from p-aminophenyl phosphinic acid derivatives is significantly reduced com
26 competitive antagonist 3-aminopropyl(methyl)-phosphinic acid did not block the resting conductance, t
28 ogenation to yield an alpha,beta-unsaturated phosphinic acid ester, following which conjugate additio
29 on of these suitably protected p-aminophenyl phosphinic acid esters with a 6-(bromomethyl)pteridine o
30 nd the same suitably protected p-aminophenyl phosphinic acid esters, followed by removal of protectin
32 ning carbon-phosphorus bonds (phosphonic and phosphinic acids) have found widespread use in medicine
34 lysin was prepared for comparison to a known phosphinic acid inhibitor, providing the first compariso
35 (K(i) = 41 nM) was comparable to that of the phosphinic acid (K(i) = 10 nM) even though the silanedio
36 ic acid and its analog 3-aminopropyl-(methyl)phosphinic acid mainly depended on residues Tyr102, Val1
37 sed drug design, we have discovered that the phosphinic acid moiety (P(O)(OH)R) behaves as an isoster
39 ons corroborate a reaction pathway where the phosphinic acid operates as a bifunctional catalyst in t
40 on, generated in situ from either the free H-phosphinic acid or ester, to a 2-methylene glutaric acid
41 raalkyl orthosilicate, to provide the free H-phosphinic acid or the corresponding ester, respectively
43 In this mechanism, the acidic proton of the phosphinic acid protonates the hydroxyl group, enhancing
44 cyclopent-1-ene, led to a rearranged allylic phosphinic acid rather than the desired homoallylic deri
45 r antagonist (3-aminopropyl)(diethoxymethyl) phosphinic acid shifted PPD to PPF, indicating that pres
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