Se-Methylselenocysteine hydrochloride, a precursor to Methylselenol, exhibits significant cancer chemopreventive and antioxidant activities. It is orally bioavailable and promotes apoptosis [1] [2].

Se-Methylselenocysteine hydrochloride at concentrations of 100-400 μM over a period of three days induces apoptosis in SKOV-33 cells [1]. The same compound also triggers caspase-3 mediated cell apoptosis under these conditions [1].

Se-Methylselenocysteine hydrochloride (0.2 mg/mouse; oral administration; once daily for 14 days) enhanced the antitumor activity of CDDP and cyclophosphamide in nude mice harboring human FaDu and A253 head and neck heterografts [2]. In Alzheimer's disease (AD) mouse models, consumption of Se-Methylselenocysteine hydrochloride in their drinking water (0.75 mg/kg body weight daily) for ten months reduced oxidative stress and neuroinflammation, modulated the distribution and levels of various metal ions, and decreased amyloid-beta peptide (Aβ) formation by inhibiting the expression of its precursor protein APP and β-secretase (BACE1). Additionally, it attenuated hyperphosphorylation of tau and the formation of neurofibrillary tangles (NFT) by enhancing protein phosphatase 2A (PP2A) activity, thereby preserving synaptic proteins and neuronal function, ultimately improving spatial learning and memory deficits in the AD mouse models [3].