Melanogenesis disturbance leads to several pathologies, including vitiligo disease. Ultraviolet (UV) narrowband phototherapy (308 or 311 nm) is used in treating vitiligo; however, the mechanism of phototherapy is not yet understood. Vitiligo is accompanied by three-fivefold increased de-novo synthesis of (6R)-l-erythro-5,6,7,8-tetrahydrobiopterin (H4Bip), its excess and its further oxidation can be considered as significant factors in the pathogenesis of vitiligo. (H4Bip), as the phenylalanine 4-hydroxylase coenzyme, catalyzes the oxidation of phenylalanine to tyrosine (a melanin precursor). In this context, photo-transformation of H4Bip in aqueous buffer solutions has been studied. HPLC–MS/MS has demonstrated that pterin products of H4Bip autoxidation (7,8-dihydropterin (H2Ptr), dihydroxanthopterin and pterin) predominate over biopterin products (7,8-dihydrobiopterin (H2Bip) and biopterin). We have shown that UV irradiation accelerates the autoxidation while the products of oxidative degradation of H4Bip act as photosensitizers. The distinctive feature of photooxidation of H4Bip from autoxidation is the formation of dihydropterin (Н2Ptr)2 and dihydrobiopterin (Н2Bip)2 dimers. By means of HPLC–MS/MS it was found that formation of dihydropterin dimers is the predominant process. The signal of molecular ion of the dimer (Н2Ptr)2 (m/z = 331) was almost a thousand times higher than the signal of (Н2Bip)2 (m/z = 479). The key point of the dimerization is photoexcitation (at 310–320 nm) of the intermolecular complex (qH2Ptr-Н2Ptr) generated in dark. As a result of the photoreaction azacyclobutane dimers have been formed. In the case of alternation of dark and light intervals H4Bip converted into dimers with 96 % yield. The data obtained are discussed in the context of UV-B narrowband vitiligo phototherapy.