1. Metabolic Enzyme/Protease
    Apoptosis
  2. Carbonic Anhydrase
    Apoptosis
  3. Zonisamide

Zonisamide (Synonyms: AD 810; CI 912)

Cat. No.: HY-B0124 Purity: 99.94%
Handling Instructions

Zonisamide (AD 810) is an orally active carbonic anhydrase inhibitor, with Kis of 35.2 and 20.6 nM for hCA II and hCA V, respectively. Zonisamide exerts neuroprotective effects through anti-apoptosis and upregulating MnSOD levels. Zonisamide also increases the expression of Hrd1, thereby improving cardiac function in AAC rats. Zonisamide can be used in studies of seizure, parkinson’s disease and cardiac hypertrophy.

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Zonisamide Chemical Structure

Zonisamide Chemical Structure

CAS No. : 68291-97-4

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Description

Zonisamide (AD 810) is an orally active carbonic anhydrase inhibitor, with Kis of 35.2 and 20.6 nM for hCA II and hCA V, respectively. Zonisamide exerts neuroprotective effects through anti-apoptosis and upregulating MnSOD levels. Zonisamide also increases the expression of Hrd1, thereby improving cardiac function in AAC rats. Zonisamide can be used in studies of seizure, parkinson’s disease and cardiac hypertrophy[1][2][3][4].

IC50 & Target

Ki: 35.2 nM (hCA II) , 20.6 nM (hCA V)[4].

In Vitro

Zonisamide (10, 50, 100, 200 µM; 24 h) increases viability of SH-SY5Y cells via an anti-apoptotic effect[1].
Zonisamide (100 µM; 24 h) shows neuroprotective effects in PD-cellular models. (PD: parkinson’s disease)[1].
Zonisamide (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 (0.1, 0.3, 1 μM; 24 h) inhibits cardiac hypertrophy and fibrosis in vitro[3].
Zonisamide markedly increases the expression of Hrd1 in Ang II-treated NRCMs[3].

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

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 (40 mg/kg; i.p.; single daily for 14 days) prevents seizures in FeCl3-induced chronic amygdalar seizures model[2].
Zonisamide (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 (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].

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
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

212.23

Formula

C8H8N2O3S

CAS No.
SMILES

O=S(CC1=NOC2=C1C=CC=C2)(N)=O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 250 mg/mL (1177.97 mM; Need ultrasonic)

H2O : 0.67 mg/mL (3.16 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 4.7119 mL 23.5593 mL 47.1187 mL
5 mM 0.9424 mL 4.7119 mL 9.4237 mL
10 mM 0.4712 mL 2.3559 mL 4.7119 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.08 mg/mL (9.80 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.08 mg/mL (9.80 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.08 mg/mL (9.80 mM); Clear solution

*All of the co-solvents are available by MCE.
Purity & Documentation

Purity: 99.94%

References
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Zonisamide
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HY-B0124
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