Eprinomectin API

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Eprinomectin API

 

Haorui supplies high quality Eprinomectin API produced by our GMP facility that has been successfully inspected by the FDA. We offer competitive prices and support our products with reliable technical and regulatory services.  Eprinomectin API is available from R&D to commercial quantities. Please contact us for more details.

 

  The following information is provided for general information purposes ONLY.

 

What is Eprinomectin?

The chemical name of eprinomectin is 4"-deoxy-4"-epiacetylamino-avermectin B1. It is a semi-synthetic member of the avermectin family of macrocyclic lactones and consists of a mixture of two homologous components, B1a (not less than 90%) and B1b (not more than 10%), which differ by a single methylene group at C26. The structure is shown in Figure 1. The purity of the compound used in the studies of toxicity was determined to be 95.1-99.6% by high-performnace liquid chromatography (HPLC).
 
Eprinomectin is active in animals against internal and external parasites. Its precise mode of action, in common with other avermectins, is unknown, despite many years of investigation of a
variety of compounds in this class. The effect of avermectins, including eprinomectin, is mediated via a specific, high-affinity receptor present in the target organisms. The physiological response to avermectin binding is increased membrane permeability to chloride ions, which is independent of gamma-aminobutyric acid (GABA)-mediated chloride channels. Although avermectins interact with the GABA-gated channels, they do so only at very high concentrations, i.e. about three orders of magnitude greater than that necessary to activate the
high-affinity receptor. Therefore, the action of the avermectins at the GABA-gated chloride ion channels is probably not involved in their nematocidal and insecticidal activity at therapeutic doses. Activation of the specific avermectin high-affinity receptor ultimately results in paralysis and death of the target organism (Turner & Schaeffer, 1989). The fact that much higher concentrations of these compounds are needed in mammals than in nematodes to affect neurological function may be due to lack of a specific, high-affinity site associated with
neuronal function or to the relatively poor penetration of these high-compounds into the central nervous system (Lankas & Gordon, 1989).
 

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