Ivermectin 99% Veterinary CAS 70288-86-7 Ivermectin

Ivermectin is a new type of broad-spectrum, highly effective, low-toxic antibiotic antiparasitic drug, which has a good expelling effect on parasites inside and outside the body, especially nematodes and arthropods. However, it is ineffective against tapeworms, trematodes and protozoa. The expelling and killing effect of macrolide antiparasitic drugs on nematodes and arthropods is to increase the release of the inhibitory transmitter γ-aminobutyric acid (GABA) of the insect body, open the Cl ion channel controlled by glutamate, and enhance the permeability of the nerve membrane to Cl, thereby blocking the transmission of nerve signals, and ultimately paralyzing the nerves, causing muscle cells to lose the ability to contract, thereby leading to the death of the insect body.

Ivermectin
Is a derivative of avermectin. William C. Campbell and Satoshi Omura, the discoverers of avermectin, won the 2015 Nobel Prize in Physiology or Medicine for their outstanding achievements in combating river blindness and elephantiasis with their derivative ivermectin.
Ivermectin is a semi-synthetic macrolide multi-component antibiotic produced by fermentation of Streptomyces avermitilis. It mainly contains ivermectin B1 (Bla+B1b) not less than 93%, of which Bla must not be less than 85%.
Ivermectin B1 is 22,23-dihydroavermectin B1.

Ivermectin is a derivative of avermectin and is an oral semi-synthetic broad-spectrum antiparasitic drug. This product is effective against most nematodes (but not all nematodes) of various life cycles; it is effective against microfilariae of Onchocerca volvulus, but not against adults; it is also effective against strongyloides that are only in the intestine. This product has a selective inhibitory effect, binding with high affinity to chloride ion channels with glutamate as valves in invertebrate nerve cells and muscle cells, thereby increasing the permeability of cell membranes to chloride ions, causing hyperpolarization of nerve cells or muscle cells, and paralyzing or killing parasites. This product can also interact with chloride ion channels of other ligand valves (such as the neurotransmitter g-aminobutyric acid (GABA)). The selectivity of this product is because some mammals do not have glutamate-chloride ion channels in their bodies, and avermectin has only low affinity for mammalian ligand-chloride ion channels. This product cannot penetrate the human blood-brain barrier. Onchocerciasis and strongyloidiasis and infections with hookworms, roundworms, whipworms, and pinworms.