TLRs are cellular receptors for microbial products that induce inflammatory responses through activation of the innate immune system.As with other quinoline antimalarial drugs, the antimalarial mechanism of action of quinine  has not been fully resolved. The most accepted model is based on hydrochloroquinine and involves the inhibition of hemozoin biocrystallization, which facilitates the aggregation of cytotoxic heme. Free cytotoxic heme accumulates in the parasites, causing death.Hydroxychloroquine increases the risk of low blood sugar through several mechanisms. These include decreased clearance of the hormone insulin from the blood, increased insulin sensitivity, and increased release of insulin from the pancreas. History
After World War I, the German government sought alternatives to quinine as an anti-malarial. Chloroquine, a synthetic analogue with the same mechanism of action was discovered in 1934, by Hans Andersag and coworkers at the Bayer laboratories. : 130–131  This was introduced into clinical practice in 1947 for the prophylactic treatment of malaria. Researchers subsequently attempted to discover structural analogs with superior properties and one of these was hydroxychloroquine. Chemical synthesis
The first synthesis of hydroxychloroquine was disclosed in a patent filed by Sterling Drug in 1949. In the final step, 4,7-dichloroquinoline was reacted with a primary amine which in turn had been made from the chloro-ketone shown:

Society and culture
It is frequently sold as a sulfate salt known as hydroxychloroquine sulfate. In the sulfate salt form, 200 mg is equal to 155 mg of the pure form.Brand names of hydroxychloroquine include Plaquenil, Hydroquin, Axemal (in India), Dolquine, Quensyl, and Quinoric. COVID-19
References
External links

"Hydroxychloroquine". Drug Information Portal.
Detection
Hydroxychloroquine may be quantified in plasma or serum to confirm a diagnosis of poisoning in hospitalized victims or in whole blood to assist in a forensic investigation of a case of sudden or unexpected death. Plasma or serum concentrations are usually in a range of 0.1-1.6 mg/L during therapy and 6–20 mg/L in cases of clinical intoxication, while blood levels of 20–100 mg/L have been observed in deaths due to acute overdosage. Interactions
The drug transfers into breast milk. There is no evidence that its use during pregnancy is harmful to the developing fetus and its use is not contraindicated in pregnancy.The concurrent use of hydroxychloroquine and the antibiotic azithromycin appears to increase the risk for certain serious side effects with short-term use, such as an increased risk of chest pain, congestive heart failure, and mortality from cardiovascular causes. Care should be taken if combined with medication altering liver function as well as aurothioglucose (Solganal), cimetidine (Tagamet) or digoxin (Lanoxin). Hydroxychloroquinecan increase plasma concentrations of penicillamine which may contribute to the development of severe side effects. It enhances hypoglycemic effects of insulin and oral hypoglycemic agents. Dose altering is recommended to prevent profound hypoglycemia. Antacids may decrease the absorption of hydroxychloroquine.