66400-12-2

Usage

Type of compound

Derivative of barbituric acid

Primary uses

Anticonvulsant and sedative medication

Mechanism of action

Enhances the effects of gamma-aminobutyric acid (GABA) in the brain

Effects

Calming and sedative

Administration methods

Intravenously or intramuscularly

Medical applications

Treatment of seizures and epilepsy

Habit-forming potential

Yes, habit-forming

Supervision

Should only be used under the supervision of a healthcare professional

Upstream product

• 75-31-0 isopropylamine 
• 1663-67-8 malonoyl dichloride 
• 141-82-2 malonic acid 
• 693-13-0 diisopropyl-carbodiimide 

Downstream Products

• 329014-86-0 5-{(4-hydroxy-phenylamine)-methylene}-1,3-diisopropyl-pyrimidine-2,4,6-trione 
• 329014-83-7 5-{(4-propargyloxy-phenylamine)-methylene}-1,3-diisopropyl-pyrimidine-2,4,6-trione 
• 329014-82-6 5-{[4-(2-ethyl-hexyloxy)-phenylamine]-methylene}-1,3-diisopropyl-pyrimidine-2,4,6-trione 
• 329014-87-1 5-{(2,4-dihydroxy-phenylamine)-methylene}-1,3-diisopropyl-pyrimidine-2,4,6-trione 

Relevant academic research and scientific papers

C-H Acidity of Barbituric Acids

The C-5-acidity of barbituric acids is correlated with the rates of proton transfer to and from that carbon atom.

An Original L-shape, Tunable N-Heterocyclic Carbene Platform for Efficient Gold(I) Catalysis

The synthesis and characterization of original NHC ligands based on an imidazo[1,5-a]pyridin-3-ylidene (IPy) scaffold functionalized with a flanking barbituric heterocycle is described as well as their use as tunable ligands for efficient gold-catalyzed C

Selective Inhibitors of a Human Prolyl Hydroxylase (OGFOD1) Involved in Ribosomal Decoding

Human prolyl hydroxylases are involved in the modification of transcription factors, procollagen, and ribosomal proteins, and are current medicinal chemistry targets. To date, there are few reports on inhibitors selective for the different types of prolyl hydroxylases. We report a structurally informed template-based strategy for the development of inhibitors selective for the human ribosomal prolyl hydroxylase OGFOD1. These inhibitors did not target the other human oxygenases tested, including the structurally similar hypoxia-inducible transcription factor prolyl hydroxylase, PHD2.

PROLYL HYDROXYLASE INHIBITORS

The invention described herein relates to certain pyrimidinetrione N-substituted glycine derivatives of formula (I), (I) which are antagonists of HIF prolyl hydroxylases and are useful for treating diseases benefiting from the inhibition of this enzyme, anemia being one example.

Pyrimidine-2,4,6-trione light screening compositions

The present invention provides compounds of formula I, which are effective in absorbing ultraviolet radiation and can be used as sunscreen agents: wherein R1and R2are each independently C2-C18alkyl, C5/sub

Barbituric acids as carbon acids. Acidity relationships and 1H and 2H transfer in 1,3-dimethyl-5-tert-butyl- and 5-tert-butylbarbituric acids

Slow ionization and reprotonation at the C5 carbon atom has been observed for 1,3-dimethyl-5-tert-butyl- (1,3-Me2-5-t-Bu), 5-tert-butyl- (5-t-Bu), 1,3-diisopropyl-(1,3-iPr2), and 1,5-diisopropyl- (1,5-i-Pr2) barbituric acids (BA) in aqueous solution at 25.0 deg C and I = 0.1 mol/dm3 (NaCl).For 1,3-Me2-5-t-Bu(BA) (pK = 9.41) deprotonation follows the rate law kf = k1H2O + k1OH-> with k1H2O = 4.0E-4/s, k1OH = 192 dm3/mol.s and reprotonation the rate law kr = k-1H2O + k-1H+> with k-1H2O = 8.9E-3/s, k-1H = 1.12E6 dm3/mol.s (pH range 6.91-12.89).For the 2H(C5) derivative the corresponding dedeuteration rates are k1H2O = 7.7E5/s (kH/kD = 5.5) and K1OH = 54 dm3/mol.s (kH/kD = 3.5).Deprotonation is catalysed by general bases (kB dm3/mol.s, kH/kD), 2,6-lutidine (0.0108, 10.0), dabco (29.6, 5.5), NH3 (1.06, 7.1), EtNH2 (14.7, 5.8), Et2NH (18.0,7.2), Et3N(1.30,7.2), but a linear correlation with pKBH is not observed, and structural effects appear to play an important role.The measurement of precise primary kinetic isotope ratios (kH/kd) in water is discussed.In 5-t-Bu(BA)(KH3) ionization at C5 (pK = 8.09+/-0.12) to produce the enolate anion (EH2-) comes into competition with ionization at imide nitrogen (pK = 7.88 +/- 0.04) to produce the keto monoanion (KH2-).In strongly alkaline solution the species deprotonated at both imide nitrogen centers (KH2- is preferred by about 20:1 over the enolate dianion (EH2-)) (C5, and imide nitrogen deprotonated).Such ionizations complicate a study of proton exchange at C5 but this has been clarified by use of the 2H(C5) substituted acid (KDH2)).Deprotonation at C5 occurs via pH independent (k1H2O = 2.59E-3/s, kH/D = 8.1) and OH(1-) dependent (k1OH = 800 dm3/mol.s, kH/kD = 3.4) reactions and via the OH(1-) dependent reactions of KH2(1-) (k2OH = 0.54 dm3/mol.s).Coresspondigly, pathways for reprotonation of the enolate anions are available through the H(1+) dependent (k-1H = 3.2E5 dm3/mol.s) and pH independent (k-1H2O = 1.62E-3/s) reactions of EH1- and through the pH independent reaction of EH(2-) (k-2H2O ca. 0.4/s).The known rates of C5 deprotonation (k1H2O) and reprotonation (k-1H) for barbituric acids have been correlated with carbon acidity (Kc) via linear Broenstead relationships of slope 0.80 and 0.20, respectively (pKc range 2.2-9.6).Barbituric acid carbon acidity is thus demonstrated to be controlled largely by substituent effects on the deprotonation reaction.