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Aminolevulinic acid phosphate is a topically administered metabolic precursor of protoporphyrin IX. After topical administration, aminolevulinic acid (ALA) is converted to protoporphyrin IX (PpIX), a photosensitizer. When the proper wavelength of light activates protoporphyrin IX, singlet oxygen is produced, resulting in a local cytotoxic effect.

Aminolevulinic acid phosphate (5-ALA) is one of the natural amino acids. It is not involved in protein synthesis but is finally metabolized to heme, which composes catalase, cytochrome, or hemoglobin as a cofactor. Externally supplied 5-ALA is imported inside the cell via peptide transporter 1, which is expressed on the cell membrane and mitochondria; similar to the naturally synthesized one, it is converted to coproporphyrinogen III and then protoporphyrin IX (PPIX) and further metabolized to heme in the presence of the ferrous ions provided from the mitochondria or supplemented sodium ferrous citrate (SFC). SFC provides ferrous ions essential for 5-ALA metabolism into heme caused by ferrochelatase. Heme is metabolized to biliverdin and carbon monoxide by heme oxygenase-1 (HO-1), and biliverdin is degraded to bilirubin. Without sufficient ferrous ions, PPIX is not further converted but exported outside the cell by an ATP-binding cassette G (ABCG) transporter. In contrast, a portion of PPIX accumulates in the cell. Recently, in vitro, antiviral effects of 5-ALA against feline infectious peritonitis virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were reported, although its antiviral mechanism has not been elucidated yet[1].

Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

[1] Shizuka Hirose. “Antiviral Effects of 5-Aminolevulinic Acid Phosphate against Classical Swine Fever Virus: In Vitro and In Vivo Evaluation.” Pathogens (2022).