2. Metabolic Enzyme/Protease Apoptosis
  3. Carbonic Anhydrase Apoptosis
  4. Zonisamide sodium

Zonisamide sodium  (Synonyms: AD 810 sodium; CI 912 sodium)

Cat. No.: HY-B0124A
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Zonisamide (AD 810) sodium is an orally active carbonic anhydrase inhibitor, with Kis 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.

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Zonisamide sodium Chemical Structure

Zonisamide sodium Chemical Structure

CAS No. : 68291-98-5

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Zonisamide sodium Related Antibodies

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Description

Zonisamide (AD 810) sodium is an orally active carbonic anhydrase inhibitor, with Kis 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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Zonisamide sodium Related Antibodies

Cell Viability Assay[1]

Cell Line: SH-SY5Y cells
Concentration: 10, 50, 100, 200 µM
Incubation Time: 24 h
Result: Induced an increase of cell viability, and with the greatest effect being at 100 µM.
Exhibited neuroprotective effect on SH-SY5Y cells (PD-cellular models) when at 100 µM.

Apoptosis Analysis[1]

Cell Line: SH-SY5Y cells
Concentration: 100 µM
Incubation Time: 24 h
Result: Showed an effect of anti-apoptotic.

RT-PCR[3]

Cell Line: NRCMs and cardiac fibroblasts (expose to Ang II for cardiomyocyte hypertrophy and fibrosis model)
Concentration: 0.1, 0.3, 1 μM
Incubation Time: 24 h
Result: Decreased the expression of atrial natriuretic factor (ANF) and cardiomyosin heavy chain β (β-MHC) but increased the expression of cardiac myosin heavy chain α (α-MHC) in NRCMs.
Decreased cardiac expression of the fibrosis-related gene Collagen 1A1 (Col1A1) in cardiac fibroblasts.

Western Blot Analysis[1]

Cell Line: SH-SY5Y cells
Concentration: 100 µM
Incubation Time: 24 h
Result: Reduced the proapoptotic molecules levels of cleaved caspase-9, -3, and p-JNK, and blocked the activation of proapoptotic molecules in SH-SY5Y cells.
Induced an increase in MnSOD levels.(MnSOD over-expression attenuates MPTP toxicity and protects cells from apoptosis).
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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male Wistar rats (200-250 g; FeCl3-induced chronic amygdalar seizures)[2].
Dosage: 40 mg/kg
Administration: Intraperitoneal injection; single daily for 14 days.
Result: Showed activity of anti-seizures.
Significantly down-regulated GABA transporters GAT-1 in the hippocampus.
Animal Model: Adult male Sprague-Dawley rats (100-120 g; cardiac hypertrophy model)[3].
Dosage: 14, 28, 56 mg/kg (dissolved in 1% DMSO)
Administration: Intraperitoneal injection; single daily for 6 weeks.
Result: Significantly attenuated cardiac hypertrophy and fibrosis.
Increased LV ejection fraction (EF), fractional shortening (FS) and E/A ratio.
Markedly increased the expression of Hrd1 in the hearts of AAC rats.
Clinical Trial
Molecular Weight

234.21

Formula

C8H7N2NaO3S
CAS No.
SMILES

O=S(CC1=NOC2=C1C=CC=C2)([NH-])=O.[Na+]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Zonisamide sodium Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Zonisamide68291-98-5AD 810CI 912AD810AD-810CI912CI-912Carbonic AnhydraseApoptosisCarbonate dehydrataseparkinson’s diseaseseizureepilepsySH-SY5YNRCMscardiac fibroblastscardiac hypertrophyInhibitorinhibitorinhibit

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