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The toxicokinetic behaviour of beta-alanine was derived on the basis of the available information. Beta-alanine is not used in the biosynthesis of any major proteins or enzymes. It is formed in-vivo by the degradation of dihydrouracil and carnosine. It 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. Beta-alanine is the rate-limiting precursor of carnosine, which means that carnosine levels are limited by the amount of available beta-alanine. Once produced in the liver, beta-alanine is taken up by several tissues, including skeletal muscle. 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. The fate of the predicted metabolites was predicted on the basis of their chemical structure based on expert judgement. Beta-alanine is expected to be highly bioavailable via the oral route but will be poorly absorbed via the dermal route. The OECD QSAR Application Toolbox predicted 3 hepatic metabolites and 3 dermal metabolites, while no gastrointestinal metabolites were predicted. Among these metabolites, malonic acid and propanoic acid were predicted in skin and liver. This prediction is in agreement with the fact that 4-Aminobutyrate aminotransferase (GABT) catalyzes the conversion of beta-alanine to malonic semialdehyde that takes part in propionate metabolism. Beta-alanine and its metabolites are soluble in water and thus subject to renal elimination. Significant faecal excretion of beta-alanine is not expected.