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Propionylcarnitine

PubChem CID
107738
Structure
Propionylcarnitine_small.png
Propionylcarnitine_3D_Structure.png
Molecular Formula
Synonyms
  • Propionylcarnitine
  • 17298-37-2
  • Propionyl carnitine
  • 3-propanoyloxy-4-(trimethylazaniumyl)butanoate
  • O-Propionylcarnitine
Molecular Weight
217.26 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-06-24
  • Modify:
    2025-01-18
Description
O-propanoylcarnitine is an O-acylcarnitine compound having propanoyl as the acyl substituent. It has a role as an analgesic, an antirheumatic drug, a cardiotonic drug, a peripheral nervous system drug and a human metabolite. It is functionally related to a propionic acid.
Propionylcarnitine has been reported in Drosophila melanogaster, Homo sapiens, and other organisms with data available.

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Propionylcarnitine.png

1.2 3D Conformer

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

3-propanoyloxy-4-(trimethylazaniumyl)butanoate
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=1S/C10H19NO4/c1-5-10(14)15-8(6-9(12)13)7-11(2,3)4/h8H,5-7H2,1-4H3
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

UFAHZIUFPNSHSL-UHFFFAOYSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

CCC(=O)OC(CC(=O)[O-])C[N+](C)(C)C
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C10H19NO4
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

2.3.2 Deprecated CAS

25518-45-0

2.3.3 ChEBI ID

2.3.4 ChEMBL ID

2.3.5 DSSTox Substance ID

2.3.6 KEGG ID

2.3.7 Lipid Maps ID (LM_ID)

2.3.8 Metabolomics Workbench ID

2.3.9 Wikidata

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • L-propionylcarnitine
  • propionyl carnitine
  • propionylcarnitine
  • propionylcarnitine, (+-)-isomer
  • propionylcarnitine, (R)-isomer

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
217.26 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3-AA
Property Value
0.9
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
0
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
4
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
6
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
217.13140809 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
217.13140809 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
66.4 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
15
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
227
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
1
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)

3.2 Chemical Classes

3.2.1 Lipids

Fatty Acyls [FA] -> Fatty esters [FA07] -> Fatty acyl carnitines [FA0707]

4 Spectral Information

4.1 Mass Spectrometry

4.1.1 GC-MS

MS Category
Experimental
MS Type
GC-MS
MS Level
MS2
Precursor Type
[M-CH3]+
Precursor m/z
202.1048
Instrument
Thermo Fisher Scientific Q Exactive GC Orbitrap GC-MS/MS
Ionization Mode
positive
Collision Energy
70
Retention Time
11.6211
Top 5 Peaks

43.05414 100

71.08549 69.85

85.1011 58.21

202.10477 56.65

121.02828 46.96

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4.1.2 MS-MS

1 of 2
NIST Number
1006045
Instrument Type
IT/ion trap
Collision Energy
0
Spectrum Type
MS2
Precursor Type
[M+H]+
Precursor m/z
218.1387
Total Peaks
2
m/z Top Peak
85
m/z 2nd Highest
159
m/z 3rd Highest
0
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2 of 2
NIST Number
1006654
Instrument Type
IT/ion trap
Collision Energy
0
Spectrum Type
MS2
Precursor Type
[M+H]+
Precursor m/z
218.1387
Total Peaks
12
m/z Top Peak
85
m/z 2nd Highest
159
m/z 3rd Highest
144
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4.1.3 LC-MS

1 of 3
View All
MS Category
Experimental
MS Type
LC-MS
MS Level
MS2
Precursor Type
[M-H]-
Precursor m/z
216.1241321
Instrument
Thermo Q Exactive HF
Instrument Type
LC-ESI-QFT
Ionization Mode
negative
Collision Energy
HCD (NCE 20-30-40%)
Top 5 Peaks

73.02952 100

201.10072 17.20

59.01365 6.70

58.00587 6.20

216.0769 5.70

Thumbnail
Thumbnail
2 of 3
View All
MS Category
Experimental
MS Type
LC-MS
MS Level
MS2
Precursor Type
[M-H]-
Precursor m/z
216.1241321
Instrument
Thermo Q Exactive HF
Instrument Type
LC-ESI-QFT
Ionization Mode
negative
Collision Energy
HCD (NCE 20-30-40%)
Top 5 Peaks

73.02949 100

216.0751 32.70

201.10031 21.40

59.01362 8.50

101.0246 7.20

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4.1.4 Other MS

1 of 3
View All
MS Category
Experimental
MS Type
Other
Precursor Type
M+H
Precursor m/z
218.139
Instrument
Orbitrap
Ionization Mode
positive
Retention Time
CCS:
Top 5 Peaks

159.064865 100

85.028046 95.82

144.101578 4.28

85.03434 4.24

159.081024 3.71

Thumbnail
Thumbnail
2 of 3
View All
MS Category
Experimental
MS Type
Other
Precursor Type
M+Na
Precursor m/z
240.121
Instrument
Orbitrap
Ionization Mode
positive
Retention Time
CCS:
Top 5 Peaks

181.046921 100

198.939026 4.44

181.064438 4.37

165.800476 3.68

73.688545 3.64

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6 Chemical Vendors

7 Drug and Medication Information

7.1 Therapeutic Uses

L-Carnitine, acetyl-L-carnitine, and/or propionyl-L-carnitine may be used for replacement therapy to restore normal carnitine concn and/or a normal nonesterified-to-esterified carnitine ratio ...
Coates, P.M., Blackman, M.R., Cragg, G.M., Levine, M., Moss, J., White, J.D. (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 76 (2005)
/EXPL THER/ The aim of this double-blind, placebo-controlled, dose titration, multicenter trial was to assess the efficacy and safety of propionyl-carnitine in intermittent claudication. ... After a 2-week preliminary period to assess maximal walking distance, 245 patients were randomly assigned to receive propionyl-L-carnitine (n = 118) or placebo (n = 127). The initial oral dose of 500 mg twice daily was increased at 2-month intervals to 2 g/day and then to 3 g/day in patients showing improvement in treadmill performance < 30% over baseline. Efficacy analysis was conducted for the 214 patients who completed the 24 weeks of treatment by comparing the effect of placebo and propionyl-L-carnitine on day 180. ... Analysis of variance showed a significant improvement of 73 +/- 9% (mean +/- SE) in maximal walking distance with propionyl-L-carnitine (n = 99) compared with 46 +/- 6% for placebo (n = 115, p = 0.03). For distance walked at onset of claudication, propionyl-L-carnitine showed about double the improvement of placebo; however, the difference was not statistically significant. There were no changes in electrocardiographic and routine biochemical and hematologic tests that would indicate an adverse effect of propionyl-L-carnitine. Adverse events requiring drug discontinuation (11 in the propionyl-L-carnitine group, 3 in the placebo group) were unrelated to study medication. The dose titration design of the study also provided information on the dose-response relation. Slightly less than 67% of patients were expected to improve their maximal walking distance by at least 30%, assuming 2 g/day of propionyl-L-carnitine (95% confidence interval 0.51 to 0.70). The response rate during the entire titration course was significantly in favor of propionyl-L-carnitine compared with placebo. ...
Brevetti G et al; J Am Coll Cardiol 26 (6):1411-6 (1995)
/EXPL THER/ Propionyl-l-carnitine (PLC) is a naturally occurring compound that has been considered for the treatment of many forms of cardiomyopathies.
Sayed-Ahmed MM et al; Pharmacol Res 43(6): 513-20 (2001)
/EXPL THER/ Propionyl-L-carnitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. ... The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with propionyl-L-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-L-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-L-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.
Ferrari R et al; Ann N Y Acad Sci 1033:79-91 (2004)
For more Therapeutic Uses (Complete) data for PROPIONYL-L-CARNITINE (13 total), please visit the HSDB record page.

7.2 Drug Warnings

Propionyl-L-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity.
Ferrari R et al; Ann N Y Acad Sci 1033:79-91 (2004)
... the efficacy and safety of oral vitamin E and propionyl-L-carnitine, separately or in combination, /were compared/ for the treatment of Peyronie's disease. ... A total of 236 men (mean age 43.4 years) with Peyronie's disease were randomly assigned to 4 groups. Group 1 (58 men) received 300 mg vitamin E orally twice daily. Group 2 (59) received 1 gm propionyl-L-carnitine orally twice daily, and group 3 (60) received 300 mg vitamin E and 1 gm propionyl-L-carnitine orally twice daily. Group 4 (control group, 59 men) received a similar regimen of placebo during the 6-month treatment period. . ... This study did not show significant improvement in pain, curvature or plaque size in patients with PD treated with vitamin E, propionyl-L-carnitine, or vitamin E plus propionyl-L-carnitine compared with those treated with placebo. Publication
Safarinejad MR et al; J Urol 178 (4 Pt 1): 1398-403; discussion 1403 (2007)

8 Food Additives and Ingredients

8.1 Associated Foods

9 Pharmacology and Biochemistry

9.1 MeSH Pharmacological Classification

Cardiotonic Agents
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)
Anti-Inflammatory Agents, Non-Steroidal
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. (See all compounds classified as Anti-Inflammatory Agents, Non-Steroidal.)

9.2 Bionecessity

Two types of carnitine deficiency states exist. Primary carnitine deficiency is a genetic disorder of the cellular carnitine-transporter system that usually manifests itself by five years of age with symptoms of cardiomyopathy, skeletal-muscle weakness, and hypoglycemia. Secondary carnitine deficiencies may occur due to certain disorders (such as chronic renal failure) or under particular conditions (eg use of certain antibiotics) that reduce carnitine absorption or increase its excretion. /Carnitine/
NIH/ODS; Dietary Supplement Fact Sheets on Carnitine (6/15/2006). Available from, as of February 26, 2008: https://ods.od.nih.gov/factsheets/carnitine.asp
Carnitine plays a critical role in energy production. It transports long-chain fatty acids into the mitochondria so they can be oxidized ("burned") to produce energy. It also transports the toxic compounds generated out of this cellular organelle to prevent their accumulation ... For genetic or medical reasons, some individuals (such as preterm infants), cannot make enough, so for them carnitine is a conditionally essential nutrient. Healthy children and adults do not need to consume carnitine from food or supplements, as the liver and kidneys produce sufficient amounts from the amino acids lysine and methionine to meet daily needs. /Carnitine/
NIH/ODS; Dietary Supplement Fact Sheets on Carnitine (6/15/2006). Available from, as of February 26, 2008: https://ods.od.nih.gov/factsheets/carnitine.asp
HIV-infected individuals often accumulate fat in some areas of the body and lose fat in others and develop high levels of blood fats (hyperlipidemia) and insulin resistance, which together constitute the lipodystrophy syndrome. This syndrome may represent mitochondrial toxicity brought about by the HIV infection and the antiretroviral drugs used to treat it, and can induce a carnitine deficiency that limits mitochondrial fat metabolism. /Carnitine/
NIH/ODS; Dietary Supplement Fact Sheets on Carnitine (6/15/2006). Available from, as of February 26, 2008: https://ods.od.nih.gov/factsheets/carnitine.asp
Carnitine homeostasis (balance within the body) among individuals with renal diseases can be substantially impaired by several factors, particularly reduced synthesis and increased elimination of the compound by the kidneys as well as reduced intake from food due to poor appetite and consumption of fewer animal products. Many patients with end-stage renal disease, particularly those on hemodialysis, become carnitine insufficient. Carnitine blood levels and muscle stores are low, which may contribute to anemia, muscle weakness, fatigue, altered levels of blood fats, and heart disorders. /Carnitine/
NIH/ODS; Dietary Supplement Fact Sheets on Carnitine (6/15/2006). Available from, as of February 26, 2008: https://ods.od.nih.gov/factsheets/carnitine.asp
For more Bionecessity (Complete) data for PROPIONYL-L-CARNITINE (7 total), please visit the HSDB record page.

9.3 Absorption, Distribution and Excretion

Most (54-86%) dietary carnitine is absorbed in the small intestine and enters the bloodstream. The kidneys efficiently conserve carnitine, so even carnitine-poor diets have little impact on the body's total carnitine content. Rather than being metabolized, excess carnitine is excreted in the urine as needed via the kidneys to maintain stable blood concentrations. /Carnitine/
NIH/ODS; Dietary Supplement Fact Sheets on Carnitine (6/15/2006). Available from, as of February 26, 2008: https://ods.od.nih.gov/factsheets/carnitine.asp
L-Carnitine and acylcarnitine esters are present in all tissues. In most tissues and cells, they are present in higher concn than in the circulation ... L-carnitine and acetyl-L-carnitine are concn in most tissues via the high-affinity, Na+-dependent organic cation transporter OCTN2 ... OCTN2 binds acetyl-L-carnitine and propionyl-L-carnitine with comparable affinity. This protein is highly expressed in heart, placenta, skeletal muscle, kidney, pancreas, testis, and epididymis and weakly expressed in brain, lung, and liver ... /Acylcarnitine esters/
Coates, P.M., Blackman, M.R., Cragg, G.M., Levine, M., Moss, J., White, J.D. (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 75 (2005)
... At a filtered load of 50 umol/L, the efficiency of L-carnitine and acylcarnitine ester reabsorption is 90 to 98% /in kidneys/. However, as the filtered load of L-carnitine incr, as, eg after consumption of a dietary supplement or after iv infusion, the efficiency of reabsorption declines rapidly ... Clearance of acylcarnitine esters is often higher than that of nonesterified L-carnitine /in kidneys/ ... Under conditions of rapid intracellular synth of acylcarnitine esters or direct accumulation from the circulation ... a higher proportion of acylcarnitine esters in urine compared to that in the circulation /is achieved/ ... Kidneys may be substantially involved in the regulation of circulating acylcarnitine ester concn. /Aacylcarnitine ester/
Coates, P.M., Blackman, M.R., Cragg, G.M., Levine, M., Moss, J., White, J.D. (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 76 (2005)
... A concn ratio of acylcarnitine esters/nonesterified L-carnitine of 0.4 or greater in plasma is ... considered abnormal ...
Coates, P.M., Blackman, M.R., Cragg, G.M., Levine, M., Moss, J., White, J.D. (Ed), Encyclopedia of Dietary Supplements. Marcel Dekker, New York, NY, p. 76 (2005)

9.4 Mechanism of Action

L-Propionylcarnitine, a propionyl ester of L-carnitine, increases the intracellular pool of L-carnitine. It exhibits a high affinity for the enzyme carnitine acetyltransferase (CAT) and, thus, is readily converted into propionyl-coenzyme A and free carnitine. It has been reported that L-propionylcarnitine possesses a protective action against heart ischemia-reperfusion injury;... To obtain a better insight into the antiradical mechanism of L-propionylcarnitine, the present research analyzed the superoxide scavenging capacity of L-propionylcarnitine and its effect on linoleic acid peroxidation. In addition, the effect of L-propionylcarnitine against DNA cleavage was estimated using pBR322 plasmid. ... L-propionylcarnitine showed a dose-dependent free-radical scavenging activity. In fact, it was able to scavenge superoxide anion, to inhibit the lipoperoxidation of linoleic acid, and to protect pBR322 DNA from cleavage induced by H2O2 UV-photolysis.
Vanella A et al; Cell Biol Toxicol 16 (2): 99-104 (2000)

9.5 Biochemical Reactions

10 Use and Manufacturing

10.1 Uses

Used to treat peripheral vascular disease
Signorelli SS et al; Clin Drug Invest 21(8): 555-561 (2001)
Free radical scavenging agent
Reznick AZ et al; Arch Biochem Biophys 296(2): 394-401 (1992)
Used therapeutically for myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism
Ferrari R et al; Ann NY Acad Sci 1033: 79-91 (2004)

11 Identification

11.1 Analytic Laboratory Methods

Analyte: propionyl-L-carnitine; matrix: bulk material; procedure: high-performance liquid chromatography with fluorescence detection at 485 nm (excitation) and 540 nm (emission); limit of detection: 100 fmole
Matsumoto K et al; J Chromatogr A 678: 241-247 (1994). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: propionyl-L-carnitine; matrix: pharmaceutical preparation (solution); procedure: high-performance liquid chromatography with ultraviolet detection at 205 nm; limit of quantitation: 185 uM
Marzo A et al; J Chromatogr 459: 313-317 (1988). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)

11.2 Clinical Laboratory Methods

Analyte: propionyl-L-carnitine; matrix: blood (plasma); procedure: high-performance liquid chromatography with fluorescence detection at 340 nm (excitation) and 475 nm (emission); limit of detection: 240 nM
Kuroda N et al; Chem Pharm Bull 44: 1525-1529 (1996). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: propionyl-L-carnitine; matrix: blood (plasma); procedure: high-performance liquid chromatography with fluorescence detection at 248 nm (excitation) and 418 nm (emission); limit of detection: 5 uM
Longo A et al; J Chromatogr B 686: 129-139 (1996). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: propionyl-L-carnitine; matrix: blood (plasma); procedure: high-performance liquid chromatography with ultraviolet detection at 260 nm; limit of detection: 10 nmole/mL
Minkler PE, Hoppel CL; Anal Biochem 212: 510-518 (1993). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
Analyte: propionyl-L-carnitine; matrix: urine; procedure: high-performance liquid chromatography with ultraviolet detection at 260 nm; limit of detection: 10 nmole/mL
Minkler PE, Hoppel CL; J Chromatogr 613: 203-221 (1993). As cited in: Lunn G; HPLC and CE Methods for Pharmaceutical Analysis. CD-ROM. New York, NY: John Wiley & Sons (2000)
For more Clinical Laboratory Methods (Complete) data for PROPIONYL-L-CARNITINE (6 total), please visit the HSDB record page.

12 Safety and Hazards

12.1 Accidental Release Measures

12.1.1 Disposal Methods

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

12.2 Regulatory Information

12.2.1 FDA Requirements

Since 1994, dietary supplements have been regulated under the Dietary Supplement Health and Education Act (DSHEA). The DSHEA requires no proof of safety for dietary supplements on the market prior to October 15, 1994. Labeling requirements for such supplements allow warnings and dosage recommendations as well as substantiated "structure or function" claims. All claims must prominently note that they have not been evaluated by the FDA, and they must bear the statement "This product is not intended to diagnose, treat, cure, or prevent any disease".
Croom EM, Walker L; Drug Topics (November 6): 84-93 (1995)

13 Toxicity

13.1 Toxicological Information

13.1.1 Interactions

Cyclosporine (CyA) is an immunosuppressive agent used after solid organ transplantation, but its clinical use is limited by side effects, the most important of which is nephrotoxicity. ... A previous work ... demonstrated that L-propionylcarnitine (L-PC), a propionyl ester of L-carnitine, is able to prevent CyA-induced acute nephrotoxicity reducing lipid peroxidation in the isolated and perfused rat kidney. CyA administration was associated with a dose dependent increase in renovascular resistance prevented by a pretreatment with L-PC. The aim of the present study was to confirm L-PC protective effect ... in an in vivo rat model. Chronic nephrotoxicity study was carried out for 28 days. L-PC was administered (ip 25 mg/kg bw) since the first day, while CyA treatment was performed for the last 21 days (by oral administration 25 mg/kg bw). ... L-PC was able to significantly lower blood pressure in CyA treated animals and to prevent CyA induced decrease in creatinine clearance. Moreover renal tissue analysis revealed that L-PC was able to reduce lipid hydroperoxide content and morphological abnormalities associated to chronic CyA administration. In conclusion our study demonstrated for the first time in vivo that L-PC protects against functional and tissue damage associated to chronic CyA administration.
Origlia N et al; Biomed Pharmacother 60 (2): 77-81 (2006)
Nephrotoxicity has represented the major limitation in the use of cyclosporine A (CyA). The structural abnormalities at the level of the proximal tubular cells are necrosis, vacuolization and lipid droplets, as well as CyA-induced glomerular afferent arteriole constriction and granular juxtaglomerular cell hyperplasia. The mode of action of vasoconstriction is not well known, but there appears to be substantial impairment of endothelial cell function leading to enhanced release of vasoconstrictors such as endothelin and thromboxane. L-propionylcarnitine (PC), one of the most potent analogues of carnitine, is able to correct and to prevent alterations in endothelial membrane permeability and it has been identified in the kidney of various animal species. To investigate a possible reduction of CyA-induced nephrotoxocity ... the effects of a pretreatment with PC before administering several doses of CyA /were examined/ n an isolated and perfused rat kidney. The histological findings showed that the perfusion with PC reduces the vasoconstrictive effect of CyA on the glomerular capillaries and preserves the tubular epithelium. The ratio of the diameter between the glomerular capillary tuft and Bowman's capsule was higher, while at the tubular level the ratio internal-diameter/diameter evaluated at the level of the basal membrane was lower in PC + CyA perfused kidneys than in only CyA perfused ones. The final value of perfusion pressure was lower in PC + CyA perfused kidneys than in only CyA perfused ones, confirming the histological findings. The release induced by CyA of alanine aminopeptidase (AAP) and N-acetyl-glucosaminidase (NAG), markers of tubular damage, was significantly reduced by pretreatment with PC. These data suggest that the pretreatment with PC reduces the CyA-induced nephrotoxicity in an isolated and perfused rat kidney.
Bertelli A et al; Drugs Exp Clin Res 21 (6): 221-8 (1005) .
The purpose of this study is to evaluate the ability of propionyl-L-carnitine, a carnitine derivative to prevent cardiac dysfunction induced by erucic acid and streptozotocin treatment in rats. Rats were fed for 10 days with normal or 10% erucic-acid-enriched diet with or without propionyl-L-carnitine injected intraperitoneally (1 mM/kg daily). Another group of rats was injected for 8-10 weeks with streptozotocin (65 mg/kg) with or without propionyl-L-carnitine intraperitoneally injected at the same dosage. Thereafter the animals were sacrificed and the hearts isolated and perfused aerobically. When isovolumic measurements of left ventricular function were applied, there was no difference in mechanical activity between treated and control hearts. On the contrary, when pressure-volume curves were determined in the paced hearts, the pressure developed by hearts from erucic acid-treated or diabetic rats was reduced. Propionyl-L-carnitine always produced positive inotropy. This was true for the control-saline treated rats that received the drug, as well as for the hearts isolated from cardiomyopathic animals. These data suggest that propionyl-L-carnitine, when given chronically, is able to overcome myocardial dysfunction caused either from erucic acid treatment or diabetes.
Pasini E et al; Am J Cardiovasc Pathol 4 (3): 216-22 (1992)
In this study, the possible mechanisms whereby propionyl-l-carnitine (PLC) could protect against adriamycin (ADR)-induced cardiomyopathy were carried out. Administration of ADR (3 mg/kg) ip, every other day over a period of 2 weeks) resulted in a significant two-fold increase in serum levels of creatine phosphokinase, lactate dehydrogenase and glutamic oxaloacetic transaminase, whereas daily administration of PLC (250 mg/kg), ip for 2 weeks) induced non-significant change. Daily administration of PLC to ADR-treated rats resulted in complete reversal of ADR-induced increase in cardiac enzymes except lactate dehydrogenase which was only reversed by 66%. In cardiac tissue homogenate, ADR caused a significant 53% increase in malonedialdehyde (MDA) and a significant 50% decrease in reduced glutathione (GSH) levels, whereas PLC induced a significant 33% decrease in MDA and a significant 41% increase in GSH levels. Daily administration of PLC to ADR-treated rats completely reversed the increase in MDA and the decrease in GSH induced by ADR to the normal levels. In rat heart mitochondria isolated 24 h after the last dose, ADR induced a significant 48% and 42% decrease in(14)CO(2)released from the oxidation of [1-(14)C]palmitoyl-CoA and [1-(14)C]palmitoylcarnitine, respectively, whereas PLC resulted in a significant 66% and 54% increase in the oxidation of both substrates, respectively. Interestingly, administration of PLC to ADR-treated rats resulted in complete recovery of the ADR-induced decrease in the oxidation of both substrates. In addition, in rat heart mitochondria, the oxidation of [1-(14)C]pyruvate, [1-(14)C]pyruvate and [1-(14)C]octanoate were not affected by ADR and/or PLC treatment. Moreover, ADR caused severe histopathological lesions manifested as toxic myocarditis which is protected by PLC. Worth mentioning is that PLC had no effect on the antitumor activity of ADR in solid Ehrlich carcinoma. Results from this study suggest that: (1) in the heart, PLC therapy completely protects against ADR-induced inhibition of mitochondrial beta -oxidation of long-chain fatty acids; (2) PLC has and/or induces a powerful antioxidant defense mechanism against ADR-induced lipid peroxidation of cardiac membranes; and finally (3) PLC has no effect on the antitumor activity of ADR.
Sayed-Ahmed MM et al; Pharmacol Res 43(6): 513-20 (2001)
For more Interactions (Complete) data for PROPIONYL-L-CARNITINE (8 total), please visit the HSDB record page.

13.1.2 Antidote and Emergency Treatment

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160-1

13.1.3 Human Toxicity Excerpts

/SIGNS AND SYMPTOMS/ At doses of approximately 3 grams/day, carnitine supplements may cause nausea, vomiting, abdominal cramps, diarrhea, and a "fishy" body odor. More rare side effects include muscle weakness in uremic patients and seizures in those with seizure disorders. /Carnitine/
NIH/ODS; Dietary Supplement Fact Sheets on Carnitine (6/15/2006). Available from, as of February 26, 2008: https://ods.od.nih.gov/factsheets/carnitine.asp

13.1.4 Non-Human Toxicity Excerpts

/OTHER TOXICITY INFORMATION/ Oxidative stress plays an important role in arterial hypertension and propionyl-L-carnitine (PLC) has been found to protect cells from toxic reactive oxygen species. ...This work ... evaluated the antioxidant capacity of chronic PLC treatment in spontaneously hypertensive rats (SHR) by measuring the activity of antioxidant enzymes and the lipid peroxidation in liver and cardiac tissues. The activity of glutathione peroxidase was decreased in liver and cardiac tissues of SHR when compared with their normotensive controls, Wistar- Kyoto (WKY) rats, this alteration being prevented by PLC treatment. Glutathione reductase activity was increased in hypertensive rats and no effect was observed after the treatment. No significant changes in superoxide dismutase activity were observed among all experimental groups. Liver of hypertensive rats showed higher catalase activity than that of normotensive rats, and PLC enhanced this activity in both rat strains. Thiobarbituric acid reactive substances, determined as a measure of lipid peroxidation, were increased in SHR compared with WKY rats, and PLC treatment decreased these values not only in hypertensive rats but also in normotensive ones. The content of carnitine in serum, liver and heart was higher in PLC-treated rats, but PLC did not prevent the hypertension development in young SHR. In addition, triglyceride levels, which were lower in SHR than WKY rats, were reduced by chronic PLC treatment in both rat strains. These results demonstrate: i) the hypotriglyceridemic effect of PLC and ii) the antioxidant capacity of PLC in SHR and its beneficial use protecting tissues from hypertension-accompanying oxidative damage.
Gomez-Anores L et al; Life Sci 78 (17): 1945-52 (2006)

13.1.5 Populations at Special Risk

Precautions: ... There are no adequate and well-controlled studies in pregnant women ... Supplemental L-carnitine should be used by pregnant women only if clearly indicated and only under medical supervision. It is not known whether L-carnitine is excreted in human milk. Supplemental L-carnitine is not advised for nursing mothers.Those with seizure disorders should only used L-carnitine under medical advisement and supervision. /L-Carnitine/
Thomson Healthcare. PDR for Nutritional Supplements. Thomson Health Care Inc. Montvale, NJ. p.258 (2001)

14 Associated Disorders and Diseases

15 Literature

15.1 Consolidated References

15.2 NLM Curated PubMed Citations

15.3 Chemical Co-Occurrences in Literature

15.4 Chemical-Gene Co-Occurrences in Literature

15.5 Chemical-Disease Co-Occurrences in Literature

16 Patents

16.1 Depositor-Supplied Patent Identifiers

16.2 WIPO PATENTSCOPE

16.3 Chemical Co-Occurrences in Patents

16.4 Chemical-Disease Co-Occurrences in Patents

16.5 Chemical-Gene Co-Occurrences in Patents

17 Interactions and Pathways

17.1 Chemical-Target Interactions

17.2 Pathways

18 Biological Test Results

18.1 BioAssay Results

19 Taxonomy

The LOTUS Initiative for Open Natural Products Research: frozen dataset union wikidata (with metadata) | DOI:10.5281/zenodo.5794106
A metabolome atlas of the aging mouse brain. Nat Commun. 2021 Oct 15;12(1):6021. DOI:10.1038/s41467-021-26310-y. PMID:34654818; PMCID:PMC8519999.
The Metabolome Atlas of the Aging Mouse Brain: https://mouse.atlas.metabolomics.us

20 Classification

20.1 MeSH Tree

20.2 ChEBI Ontology

20.3 LIPID MAPS Classification

20.4 KEGG: Lipid

20.5 ChemIDplus

20.6 ChEMBL Target Tree

20.7 UN GHS Classification

20.8 NORMAN Suspect List Exchange Classification

20.9 EPA DSSTox Classification

20.10 LOTUS Tree

20.11 MolGenie Organic Chemistry Ontology

21 Information Sources

  1. CAS Common Chemistry
    LICENSE
    The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc/4.0/
  2. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  3. EPA DSSTox
    3-(Propanoyloxy)-4-(trimethylazaniumyl)butanoate
    https://comptox.epa.gov/dashboard/DTXSID20938255
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  4. Hazardous Substances Data Bank (HSDB)
  5. ChEBI
  6. LOTUS - the natural products occurrence database
    LICENSE
    The code for LOTUS is released under the GNU General Public License v3.0.
    https://lotus.nprod.net/
  7. ChEMBL
    LICENSE
    Access to the web interface of ChEMBL is made under the EBI's Terms of Use (http://www.ebi.ac.uk/Information/termsofuse.html). The ChEMBL data is made available on a Creative Commons Attribution-Share Alike 3.0 Unported License (http://creativecommons.org/licenses/by-sa/3.0/).
    http://www.ebi.ac.uk/Information/termsofuse.html
  8. Comparative Toxicogenomics Database (CTD)
    LICENSE
    It is to be used only for research and educational purposes. Any reproduction or use for commercial purpose is prohibited without the prior express written permission of NC State University.
    http://ctdbase.org/about/legal.jsp
  9. FooDB
    LICENSE
    FooDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (FooDB) and the original publication.
    https://foodb.ca/about
  10. KEGG
    LICENSE
    Academic users may freely use the KEGG website. Non-academic use of KEGG generally requires a commercial license
    https://www.kegg.jp/kegg/legal.html
  11. LIPID MAPS
    Lipid Classification
    https://www.lipidmaps.org/
  12. Natural Product Activity and Species Source (NPASS)
  13. West Coast Metabolomics Center-UC Davis
    Propionylcarnitine
  14. MassBank of North America (MoNA)
    LICENSE
    The content of the MoNA database is licensed under CC BY 4.0.
    https://mona.fiehnlab.ucdavis.edu/documentation/license
  15. Metabolomics Workbench
  16. NIST Mass Spectrometry Data Center
    LICENSE
    Data covered by the Standard Reference Data Act of 1968 as amended.
    https://www.nist.gov/srd/public-law
  17. Wikidata
    O-propanoylcarnitine (internal charge)
    https://www.wikidata.org/wiki/Q27103933
  18. PubChem
  19. Medical Subject Headings (MeSH)
    LICENSE
    Works produced by the U.S. government are not subject to copyright protection in the United States. Any such works found on National Library of Medicine (NLM) Web sites may be freely used or reproduced without permission in the U.S.
    https://www.nlm.nih.gov/copyright.html
    Anti-Inflammatory Agents, Non-Steroidal
    https://www.ncbi.nlm.nih.gov/mesh/68000894
  20. GHS Classification (UNECE)
  21. NORMAN Suspect List Exchange
    LICENSE
    Data: CC-BY 4.0; Code (hosted by ECI, LCSB): Artistic-2.0
    https://creativecommons.org/licenses/by/4.0/
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  22. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  23. PATENTSCOPE (WIPO)
CONTENTS