| Customization: | Available |
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| Powder: | Yes |
| Customized: | Negotiable |
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| Product name | Chloroquine Phosphate |
| CAS No. | 50-63-5 |
| EINECS | 200-055-2 |
| Mf | C18H32ClN3O8P2 |
| Mw | 515.86 |
Pharmacology and toxicology
(1) Pharmacodynamics: Chloroquine can cause the nuclear fragmentation of malaria parasites, the emergence of vacuoles between cells, and the aggregation of malaria pigments into clumps. It is known that chloroquine can not directly kill the malaria parasite, but can interfere with its reproduction, the mechanism of action is that this product has a strong binding force with nuclear protein, inserted into the double helix of DNA between the two strands, can form a complex with DNA, thereby preventing DNA replication and RNA transcription. Chloroquine also inhibits the incorporation of into the DNA and RNA of the malaria parasite and interferes with its reproduction. Chloroquine accumulates in large quantities in infected red blood cells and is concentrated in food vesicles and lysosomes of protozoa. The loss of hemoglobin protease, which digests hemoglobin, makes the parasite unable to digest the ingested hemoglobin, resulting in the deficiency of amino acids necessary for the growth and development of the parasite, and causes the breakdown of ribonucleic acid. In addition, chloroquine can also interfere with the entry of fatty acids into phospholipids, control glutamate dehydrogenase and hexokinase. Chloroquine mainly acts on the schizozoites of the red endphase, and after 48 to 72 hours, the schizozoites in the blood are killed. This product is ineffective for the infrared phase of vivax malaria, so it can not cure vivax malaria. Falciparum malaria can be cured. Chloroquine also has no direct effect on gametophytes, so it cannot be used for etiological prevention and interruption of transmission.
Experiments with tritium-labeled chloroquine showed that chloroquine-resistant Plasmodium falciparum released chloroquine 40 to 50 times faster than sensitive Plasmodium falciparum. This change was caused by mutations in Plasmodium falciparum genes. After years of research, the gene for resistance to chloroquine in malaria parasites has been discovered. This gene is located on a 36kb DNA segment in chromosome 7 of malaria parasites, called the Cg2 gene, which has complex polymorphisms. The Cg2 gene contains 12 significant mutation sites and 3 polymorphic repeats, of which 4 to 8 have minor mutations that are sufficient to make the parasite resistant to chloroquine.
pharmacokinetics
After oral administration, the intestinal absorption of chloroquine is fast and adequate, and the blood concentration is the highest 1 to 2 hours after taking the drug. About 55% of drugs are in the blood bound to plasma components. The blood concentration was maintained for a long time, the half-life (t1/2) was 2.5~10 days, the concentration of chloroquine in red blood cells was 10~20 times that of plasma, and the concentration of chloroquine in red blood cells invaded by plasmodium was about 25 times higher than that of normal people. Chloroquine binds more to histamin, and its concentration in liver, spleen, kidney, and lung is up to 200 times higher than that in plasma. The concentration in brain tissue and spinal cord tissue is 10-30 times that of plasma concentration. The metabolic transformation of chloroquine in vivo is carried out in the liver, and its main metabolite is deethylchloroquine, which still has antimalarial effects. A small amount (10%-15%) of chloroquine is excreted in its original form through the kidney, and its excretion rate can be accelerated by urine acidification and reduced by alkalination. About 8% is excreted in the stool, and chloroquine can also be excreted from the milk.
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