Zonisamide (sodium)

Zonisamide (AD 810) sodium is an orally active carbonic anhydrase inhibitor, with K_is of 35.2 and 20.6 nM for hCA II and hCA V, respectively. Zonisamide sodium exerts neuroprotective effects through anti-apoptosis and upregulating MnSOD levels. Zonisamide sodium also increases the expression of Hrd1, thereby improving cardiac function in AAC rats. Zonisamide sodium can be used in studies of seizure, parkinson’s disease and cardiac hypertrophy^[1][2][3][4]. IC50 & Target: Ki: 35.2μM (hCA II) , 20.6 nM (hCA V)^[2] In Vitro: Zonisamide sodium (10, 50, 100, 200 µM; 24 h) increases viability of SH-SY5Y cells via an anti-apoptotic effect^[1].
Zonisamide sodium (100 µM; 24 h) shows neuroprotective effects in PD-cellular models. (PD: parkinson’s disease)^[1].
Zonisamide sodium (100 µM; 24 h) reduces levels of proapoptotic molecules, and upregulates levels of MnSOD (MnSOD over-expression attenuates MPTP toxicity and protects cells from apoptosis)^[1].
Zonisamide sodium (0.1, 0.3, 1 μM; 24 h) inhibits cardiac hypertrophy and fibrosis in vitro^[3].
Zonisamide sodium markedly increases the expression of Hrd1 in Ang II-treated NRCMs^[3]. In Vivo: Zonisamide sodium (40 mg/kg; i.p.; single daily for 14 days) prevents seizures in FeCl₃-induced chronic amygdalar seizures model^[2].
Zonisamide sodium (14, 28, 56 mg/kg; i.p.; single daily for 6 weeks) alleviates cardiac hypertrophy and improved cardiac function in rats subjected to AAC (abdominal aortic constriction)^[3].
Zonisamide sodium (14, 28, 56 mg/kg; i.p.; single daily for 6 weeks) upregulates Hrd1 expression and accelerates ERAD in the hearts of AAC rats^[3].