Methyl aminolevulinate (hydrochloride)

Methyl aminolevulinate hydrochloride is a sensitizer used in photodynamic therapy (PDT). Methyl aminolevulinate hydrochloride penetrates the skin and induces the production of photoactive porphyrins including protoporphyrin IX in cells; upon exposure to appropriate light, it generates ROS, which triggers cellular oxidation and cell death. Methyl aminolevulinate hydrochloride acts as a photo-damage reversing agent through epidermal reconstruction, cytokine-mediated activation of dermal fibroblasts, elastin breakdown, new collagen formation, and compression of dilated capillaries. Methyl aminolevulinate hydrochloride reduces the expression of the proliferation marker K_i-67 and the early skin carcinogenesis marker TP53. Methyl aminolevulinate hydrochloride delays the onset of ultraviolet-induced skin tumors and reduces tumor burden in hairless mice. Methyl aminolevulinate hydrochloride is applicable to research related to actinic keratosis and basal cell carcinoma^[1][2]. In Vitro:Methyl aminolevulinate (0.0001-1.4 mmol/L) hydrochloride induces concentration-dependent formation of photoactive porphyrins in cultures of mouse adenocarcinoma LM2 cells, with the highest yield of 48 ng/10⁵ cells observed at the concentration of 1.4 mmol/L; additionally, 90% of porphyrins remain intracellular at all tested concentrations^[1].
Methyl aminolevulinate (1.2-1.8 mmol/L, 3 h) hydrochloride shows no intrinsic cytotoxicity against mouse adenocarcinoma LM2 cells at the concentration of 1.8 mmol/L, but induces 98% cell death when cells are treated with 1.2 mmol/L for 3 h followed by irradiation with 3 J/cm^2[1]. In Vivo:Methyl aminolevulinate (8-20%; topical administration; once weekly; administered to UV-exposed mice for 26 weeks; administered to non-UV-exposed mice for up to 36 weeks) hydrochloride significantly delays the onset time of UV-induced skin tumors and reduces tumor burden in hairless mice, and selectively accumulates photoactive porphyrins in UV-induced skin tumors^[1].