1. 2,2-dimethylpropionic Acid
2. Pivalic Acid, Sodium Salt
1. 75-98-9
2. Trimethylacetic Acid
3. 2,2-dimethylpropanoic Acid
4. 2,2-dimethylpropionic Acid
5. Neopentanoic Acid
6. Tert-pentanoic Acid
7. Propanoic Acid, 2,2-dimethyl-
8. Versatic 5
9. Kyselina Pivalova
10. Acetic Acid, Trimethyl-
11. 2,2-dimethyl-propionic Acid
12. Alpha,alpha-dimethylpropionic Acid
13. Dimethylpropionic Acid
14. Acide Pivalique
15. Acido Pivalico
16. Kyselina 2,2-dimethylpropionova
17. Neovaleric Acid
18. Propionic Acid, 2,2-dimethyl-
19. Nsc 65449
20. 2,2-dimethyl-propanoic Acid
21. Tert-c4h9cooh
22. Acide 2,2-dimethylpropanoique
23. Chebi:45133
24. 813re8bx41
25. Nsc-65449
26. .alpha.,.alpha.-dimethylpropionic Acid
27. Kyselina Pivalova [czech]
28. Hsdb 5211
29. Einecs 200-922-5
30. Brn 0969480
31. Kyselina 2,2-dimethylpropionova [czech]
32. Pivalinsaeure
33. Pivalinsaure
34. Pivaloic Acid
35. Unii-813re8bx41
36. Ai3-04165
37. Pvalc Acd
38. Pivalic Acid;
39. Pivoh
40. Piv
41. Trimethyl Acetic Acid
42. Trimethyl-acetic Acid
43. Pivalic Acid, 99%
44. Dsstox_cid_6432
45. Tert-butyl Carboxylic Acid
46. Pivalic Acid [mi]
47. 2,2 Dimethylpropanoic Acid
48. Ec 200-922-5
49. Schembl3613
50. Dsstox_rid_78111
51. 2,2,-dimethylpropionic Acid
52. 2,2,2-trimethylacetic Acid
53. Dsstox_gsid_26432
54. 4-02-00-00908 (beilstein Handbook Reference)
55. Chembl322719
56. Zinc7993
57. Dimethylpropionic Acid (related)
58. Dtxsid8026432
59. Wln: Qvx1&1&1
60. Pivalic Acid (acd/name 4.0)
61. Baa18488
62. Cs-d1464
63. Nsc65449
64. Str05697
65. Tox21_200425
66. Lmfa01020073
67. Mfcd00004194
68. Stl264139
69. 5-iodo-mono-methylisophthalate
70. Akos000119013
71. Cas-75-98-9
72. Ncgc00248606-01
73. Ncgc00257979-01
74. Bp-30032
75. 2,2-dimethylpropanoic Acid [hsdb]
76. Ft-0656670
77. P0461
78. Pivalic Acid Solution, 1 M In Dichloromethane
79. D78007
80. A838577
81. Q421509
82. J-523981
83. F2191-0097
84. Z1258943356
| Molecular Weight | 102.13 g/mol |
|---|---|
| Molecular Formula | C5H10O2 |
| XLogP3 | 1.5 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 1 |
| Exact Mass | 102.068079557 g/mol |
| Monoisotopic Mass | 102.068079557 g/mol |
| Topological Polar Surface Area | 37.3 Ų |
| Heavy Atom Count | 7 |
| Formal Charge | 0 |
| Complexity | 78.6 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
MEDICATION (VET): Pivalic acid was shown to possess musculotropic spasmolytic activity comparable or superior to papaverine hydrochloride on a Guinea pig ileum preparation. In addition, it exhibited neurotropic spasmolytic activity as well as hypotensive activity in rabbits.
Lespagnol et al; Chim Ther 4 (2): 103 (1969)
Prodrugs that liberate pivalate (trimethylacetic acid) after hydrolysis have been developed to improve the bioavailability of therapeutic candidates. Catabolism of pivalate released by activation of a prodrug is limited in mammalian tissues. Pivalate can be activated to a coenzyme A thioester in cells. In humans, formation and urinary excretion of pivaloylcarnitine generated from pivaloyl-CoA is the major route of pivalate elimination. Because the total body carnitine pool is limited and can only slowly be replenished through normal diet or biosynthesis, treatment with large doses of pivalate prodrugs may deplete tissue carnitine content. Animal models and long-term treatment of patients with pivalate prodrugs have resulted in toxicity consistent with carnitine depletion. However, low plasma carnitine concentrations after pivalate prodrug exposure may not reflect tissue carnitine content and, thus, cannot be used as a surrogate for potential toxicity. The extent of tissue carnitine depletion will be dependent on the dose of pivalate, because carnitine losses may approximate the pivalate exposure on a stoichiometric basis. These concepts, combined with estimates of carnitine dietary intake and biosynthetic rates, can be used to estimate the impact of pivalate exposure on carnitine homeostasis. Thus, even in populations with altered carnitine homeostasis due to underlying conditions, the use of pivalate prodrugs for short periods of time is unlikely to result in clinically significant carnitine depletion. In contrast, long-term treatment with substantial doses of pivalate prodrugs may require administration of carnitine supplementation to avoid carnitine depletion.
PMID:12429869 Brass EP; Pharmacol Rev 54 (4): 589-98 (2002)
The metabolism and clinical safety of the pivalic acid-containing antibiotic S-1108, an orally active pro-drug cephalosporin, were investigated to assess the clinical effects, with special emphasis on the influence of carnitine consumption in 15 patients with various infectious diseases receiving S-1108 three times a day at a 300- or 600-mg total daily dose for 3 to 7 days. The free carnitine concentrations in plasma were greatly reduced to approximately 65% of pretreatment levels, and the plasma pivaloylcarnitine (the main metabolite of pivaloyloxymethyl ester) concentrations were increased during the 200-mg (three times a day) regimens but returned to the pretreatment levels within 3 to 5 days after the cessation of treatment. In three elderly patients with declining renal function (creatinine clearance rate, 31 to 50 ml/min), the acylcarnitine/free carnitine ratio increased from 0.1 to 0.4 up to 0.7 to 1.5 at day 5 during the 7-day treatment, showed a tendency to decrease, and then returned to the pretreatment ratio 4 days after discontinuation of the drug. The degree of free carnitine reduction and increase of the acylcarnitine/free carnitine ratio depended mostly on the dose and the duration of S-1108 treatment. The increased acylcarnitine/free carnitine ratio in elderly patients was due to reduction of the free carnitine concentration in plasma and mainly to the retardation of nontoxic pivaloylcarnitine excretion. This study indicated that there was a decrease in free carnitine levels in plasma, but there were no clinical symptoms or adverse effects associated with carnitine reduction in patients during the 7-day multiple administration of S-1108.
PMID:8517691 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC187892 Shimizu K et al; Antimicrob Agents Chemother 37 (5): 1043-9 (1993)
14(C) labeled pivalic acid, administered orally in mice, was well absorbed and distributed in bone, kidneys, olfactory bulb, salivary gland, and some adipose tissues, and finally excreted in urine, primarily as its conjugated forms.
Shindo H et al; Oyo Yakuri 17 (6): 923-33 (1979)
Both pivaloylesterified antibiotics and pivalic acid cause pivaloylcarnitine excretion into urine in the rat and human. In the present study, the formation of pivaloylcarnitine, expressed as short-chain acylcarnitines has been observed in rats. The carnitine pool of the rats was radiolabeled by injection of L-[3H]butyrobetaine 24 h prior to exposure to pivalic acid injected i.p. or pivampicillin administered orally. The presence of pivaloylcarnitine in liver, heart, kidney, stomach, small intestine, testis, muscle, brown fat, white fat and serum was determined at zero time, 0.5, 2, 8 and 24 h after exposure to pivalic acid. After injection of pivalic acid, pivaloylcarnitine calculated as percent of free carnitine and short-chain acylcarnitines amounted to (mean +/- SD) 1.1 +/- 0, 15.4 +/- 2.5, 33.4 +/- 0.7 and 37.5 +/- 1.5% in the heart and 1.2 +/- 0.2, 20.6 +/- 9.5, 29.8 +/- 7.6 and 22.5 +/- 1.6% in brown fat after 0, 0.5, 2 and 8 h, respectively. 2 h after administration, pivaloylcarnitine calculated as percent of free carnitine and short-chain acylcarnitines was highest in the heart (20.9 +/- 7.6%) and brown fat (19.0 +/- 8.5%) in the pivalic acid-treated rat, and highest in the kidney (12.4 +/- 3.1%) and brown fat (10.2 +/- 2.8%) in the pivampicillin-treated rat. Pivaloylcarnitine percent in the liver was 2.8 +/- 0.6 in the pivalic acid-treated rat, 3.5 +/- 1.2 in the pivampicillin-treated rat and 1.3 +/- 0.4 in the control group. Pivaloylcarnitine concentration, nmol/g and nmol/organ, was highest in the heart and brown fat in both treatment groups. The present study suggests that the heart and the brown fat, but not the liver, play important roles in pivaloylcarnitine formation in the rat.
PMID:7827109 Diep QN et al; Biochim Biophys Acta 1243 (1): 65-70 (1995)
Pivalic acid administered orally to mice was excreted in urine primarily in conjugated forms.
Shindo TT et al; Oyo Yakuri 17 (6): 923-33 (1979)
Three healthy volunteers were orally dosed with 100 and 200 mg of the test substance. More than 90% of pivalic acid is excreted as pivaloyl-carnitine and no measurable amount of free pivalic acid was present in the urine samples, indicating that pivalic acid was quantitatively conjugated with carnitine in the human body. /Pivaloyloxymethyl (+)-(6R,7R)-7-[(Z)-2-(2-amino-4-thiazolyl)-2-pentenamido]-3-carbamoyloxymethyl-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylate hydrochloride hydrate (S-1108), an oral cephem antibiotic/
European Chemicals Bureau; IUCLID Dataset, Pivalic acid (75-98-9) p.21 (2000 CD-ROM edition). Available from, as of January 3, 2008: https://esis.jrc.ec.europa.eu/
Healthy volunteers in a Phase I clinical study were orally dosed with 200 mg of the test substance 3 times a day for 8 days. No clinical or abnormal signs. Pivalic acid is metabolized in the body to pivaloyl-carnitine. The urinary excretion of pivaloyl-carnitine and the plasma carnitine concentration of 50% indicates that there is enough carnitine store in the body to detoxify the pivalic acid. /Pivaloyloxymethyl (+)-(6R,7R)-7-[(Z)-2-(2-amino-4-thiazolyl)-2-pentenamido]-3-carbamoyloxymethyl-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylate hydrochloride hydrate (S-1108), an oral cephem antibiotic/
European Chemicals Bureau; IUCLID Dataset, Pivalic acid (75-98-9) p.23 (2000 CD-ROM edition). Available from, as of January 3, 2008: https://esis.jrc.ec.europa.eu/
Freshly prepared rat hepatocytes from male Sprague-Dawley rats/ partly clofibrate treated, were exposed to 0, 0.5, 1.0, 5.0, and 10.0 mM of the test substance. Hepatocytes activate pivalate to pivaloyl-CoA, which can be used as a substrate for pivaloylcarnitine formation. the sequestration of hepatocyte CoA as pivaloyl-CoA is associated with the inhibition of pyruvate oxidation. /Pivalate/
European Chemicals Bureau; IUCLID Dataset, Pivalic acid (75-98-9) p.23 (2000 CD-ROM edition). Available from, as of January 3, 2008: https://esis.jrc.ec.europa.eu/
For more Metabolism/Metabolites (Complete) data for 2,2-DIMETHYLPROPANOIC ACID (9 total), please visit the HSDB record page.
BUILDING BLOCK
