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Cat. No. M4815
Vigabatrin Structure


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Quality Control
  • Current batch:
  • Purity >98%
  • COA
  • MSDS
Biological Activity

Vigabatrin was found to selectively suppress the late HFOs of ictal complexes. Vigabatrin also suppressed abnormal HFOs recorded during the interictal periods. Thus Vigabatrin was found to be effective in suppressing both the generation of spasms and hypsarrhythmia in the TTX model. Vigabatrin also appears to preferentially suppress the generation of abnormal HFOs, thus implicating neocortical HFOs in the infantile spasms disease state.Although Vigabatrin is associated with retinal dysfunction in patients and Vigabatrin toxicity has been demonstrated by other laboratories in the albino rat, in one pigmented and albino rats, Vigabatrin did not induce deficits in, but rather enhanced, retinal function. Nonetheless, retinal neuronal dysplasia was observed.

Customer Product Validations & Biological Datas
Source Int J Pharm (2014). Figure 2. Vigabatrin
Method LC–MS bioanalysis
Cell Lines Caco-2 cells
Concentrations 30 mM
Incubation Time 6 d
Results Increasing the concentration of vigabatrin to 30 mM significantly decreased the uptake of Tau to 34 ± 3%
Source Int J Pharm (2014). Figure 1. Vigabatrin
Method LC–MS bioanalysis
Cell Lines Caco-2 cells
Concentrations 30 mM
Incubation Time 6 d
Results Vigabatrin is able to concentration-dependently inhibit the uptake of the prototypic PAT1 substrate proline (Pro) under slightly acidic condition (pH 6.0) in Caco-2 cells yielding an IC50 value of 16.8 mM (logIC50 = 1.2 ± 0.2) with a Hill slope of =0.9±0.3
Cell Experiment
Cell lines Caco-2 cell
Preparation method The ability of infant formula, Trp, Gly-Gly, Gly-Sar, 2-amino-2-norbornanecarboxylic acid (BCH) and Ile to inhibit the vigabatrin transport in the A–B direction was investigated. NaCl-reduced HBSS containing 1.0 mmol/L vigabatrin and 35.0 mmol/L Trp, 20 mg mL−1 Gly-Gly (151.4 mmol/L), Gly-Sar (136.9 mmol/L), BCH (128.9 mmol/L) or Ile (152.5 mmol/L), with the osmolarity adjusted to 270–310 mOsmol L−1 with mannitol, or H2O containing 1.0 mmol/L vigabatrin and low fat infant formula (150 mg mL−1), with an osmolarity of 310–336 mOsmol L−1 was applied to the apical side of the cells.
Concentrations 1.0 mmol/L
Incubation time 24 h
Animal Experiment
Animal models Sprague-Dawley rats
Dosages 200 mg/kg/d
Administration oral
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

Chemical Information
Molecular Weight 129.16
Formula C6H11NO2
CAS Number 60643-86-9
Purity >98%
Solubility Water 19 mg/mL
Storage at -20°C

[1] Frost JD Jr, et al. Neurobiol Dis. Vigabatrin therapy implicates neocortical high frequency oscillations in an animal model of infantile spasms.

[2] Akula JD, et al. Doc Ophthalmol. Vigabatrin can enhance electroretinographic responses in pigmented and albino rats.

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Keywords: Vigabatrin, VGB supplier, GABA Receptor, inhibitors

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