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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

basic toxicokinetics
Type of information:
calculation (if not (Q)SAR)
Migrated phrase: estimated by calculation
Adequacy of study:
key study
1 (reliable without restriction)
Rationale for reliability incl. deficiencies:
other: Expert judgment is combined with the prediction of metabolism provided by OECD QSAR application Toolbox

Data source

Reference Type:
other: expert statement
Report date:

Materials and methods

Objective of study:
Test guideline
no guideline followed
Principles of method if other than guideline:
Experimental data on toxicokinetic behaviour of beta-alanine are not available. However, according to the Regulation (EC) No 1907/2006, Annex VIII, Column 1, assessment of the toxicokinetic behaviour of the substance can be derived from the relevant available information. The subject of this evaluation is therefore to derive toxicokinetic behaviour of beta-alanine. The OECD QSAR Application Toolbox was used to make a qualitative prediction of metabolites formed in liver, skin and gastrointestinal tract. The Danish QSAR Database was used to predict dermal and oral bioavailability of beta-alanine. Information about the metabolic pathways of beta-alanine is available at The fate of beta-alanine metabolites was predicted on the basis of their chemical structure based on expert judgement.
GLP compliance:
No guideline exists for this type of appraisal

Test material

Constituent 1
Chemical structure
Reference substance name:
EC Number:
EC Name:
Cas Number:
Molecular formula:
Details on test material:
not applicable

Test animals

other: not applicable

Administration / exposure

Route of administration:
other: oral route of administration is considered

Results and discussion

Main ADME resultsopen allclose all
Beta-alanine is expected to be highly bioavailable via the oral route but will be poorly absorbed via the dermal route
Once produced in the liver, beta-alanine is taken up by several tissues, including skeletal muscle.
malonic semialdehyde, malonic acid and propanoic acid were predicted in skin and liver
Beta-alanine and its metabolites are subject to renal elimination.

Toxicokinetic / pharmacokinetic studies

Details on absorption:
The Danish QSAR database predicts a low dermal absorption of 0.001 mg/cm²/event and oral absorption of 0% following a dose of 1 mg. The latter prediction is thought to be incorrect since active amino acid transport systems are expressed in the intestinal tract that are likely to facilitate the absorption of beta-alanine following oral ingestion. The oral absorption of beta-alanine is likely to be similar to that of alanine, i.e., near quantitative. Application of Lipinski's "Rule of Five" suggests that beta-alanine is indeed orally bioavailable.

Details on distribution in tissues:
Once produced in the liver, beta-alanine is taken up by several tissues, including skeletal muscle. This fate is likely to be shared by exogenous beta-alanine.
Details on excretion:
The substance and its metabolites are soluble in water (beta-alanine: 428500 mg/L, malonic acid: 1000000 mg/L ; 3-hydroxypropanoic acid: 1000000 mg/mL ) and will be excreted rapidly via urine. Significant faecal excretion of beta-alanine or its metabolites is not expected.

Metabolite characterisation studies

Metabolites identified:
not measured
Details on metabolites:
Beta-alanine is the only naturally occurring non-essential beta amino acid, endogenously produced by the liver. It is not used in the biosynthesis of any major proteins or enzymes. It is formed in organism by different metabolic pathways. One occurs via reductive pyrimidine degradation and begins with the conversion of uracil to 5,6-dihydrouracil by dihydropyrimidine dehydrogenase. Then dihydropyrimidinase catalyzes the reversible hydrolytic ring opening of dihydrouracil to N-carbamoyl-beta-alanine, which in turn is hydrolyzed to beta-alanine by beta-ureidopropionase. Another main pathway of beta-alanine biosynthesis is degradation of beta-alanyl-(L)-histidine. Carnosine N-methyltransferase converts beta-alanyl-(L)-histidine to anserine using S-adenosyl-L-methionine as methyl donor. Then anserine is hydrolyzed to beta-alanine by carnosine dipeptidase 1 (metallopeptidase M20 family) CPGL2. Beta-alanyl-(L)-histidine may also be hydrolyzed by CPGL2 to beta-alanine and (L)-histidine.
Beta-alanine is a component of the naturally occurring peptides carnosine and anserine and also of pantothenic acid (vitamin B5) which itself is a component of coenzyme A. Under normal conditions, beta-alanine is metabolized into acetic acid. In addition it is formed in-vivo by the metabolism of spermine and L-aspartate.
(L)-Aspartic acid undergoes decarboxylation to beta-alanine by glutamate decarboxylase 1 (brain, 67 kDa) and glutamate decarboxylase 2 (pancreatic islets and brain, 65 kDa) or by cysteine sulfinic acid decarboxylase.
1,3-diaminopropane is involved in the beta-alanine metabolic pathway via formation of 3-aminopropanal by amiloride binding protein 1 [amine oxidase (copper-containing)] followed by aldehyde dehydrogenase 9 family, member A1 (ALD9A1)-catalyzed oxidation to beta-alanine. 4-Aminobutyrate aminotransferase (GABT) catalyzes the conversion of 2-oxo-glutaric acid and beta-alanine to L-glutamic acid and malonic semialdehyde that takes part in propionate metabolism.
The OECD QSAR Application Toolbox predicts 3 hepatic metabolites and 3 dermal metabolites, while no gastrointestinal metabolites were predicted (malonic semialdehyde, malonic acid, and propanoic acid, 3-hydroxy-).
Among these metabolites, malonic acid and propanoic acid were predicted in skin and liver. This prediction is in agreement with the fact that gamma-aminobutyrate aminotransferase (GABT) catalyzes the conversion of beta-alanine to malonic semialdehyde that takes part in propionate metabolism.

Applicant's summary and conclusion