Against rheumatoid arthritis, it operates by inhibiting lymphocyte proliferation, phospholipase A2, antigen presentation in dendritic cells, release of enzymes from lysosomes, release of reactive oxygen species from macrophages, and production of IL-1. History
In Peru, the indigenous people extracted the bark of the Cinchona tree (Cinchona officinalis) and used the extract to fight chills and fever in the seventeenth century. In 1633 this herbal medicine was introduced in Europe, where it was given the same use and also began to be used against malaria. The quinoline antimalarial drug quinine was isolated from the extract in 1820.: 130–131 After World War I, the German government sought alternatives to quinine. Chloroquine, a synthetic analogue with the same mechanism of action was discovered in 1934, by Hans Andersag and coworkers at the Bayer laboratories, who named it Resochin. It was ignored for a decade, because it was considered too toxic for human use. Instead, in World War II, the German Africa Corps used the chloroquine analogue 3-methyl-chloroquine, known as Sontochin. After Allied forces arrived in Tunis, Sontochin fell into the hands of Americans, who sent the material back to the United States for analysis, leading to renewed interest in chloroquine. United States government-sponsored clinical trials for antimalarial drug development showed unequivocally that chloroquine has a significant therapeutic value as an antimalarial drug. : 61–66  It was introduced into clinical practice in 1947 for the prophylactic treatment of malaria. Chemical synthesis
The first synthesis of chloroquine was disclosed in a patent filed by IG Farben in 1937.
Changes in sex hormone levels, specifically elevated levels of estrogen and relaxin in females during the menstrual cycle, have been hypothesized as causing predisposition of ACL ruptures. This is because they may increase joint laxity and extensibility of the soft tissues surrounding the knee joint. Ongoing research has observed a greater occurrence of ACL injuries in females during ovulation and fewer injuries during the follicular and luteal phases of the menstrual cycle.Study results have shown that female collegiate athletes with concentration levels of relaxin that are greater than 6.0 pg/mL are at four times higher risk of an ACL tear than those with lower concentrations.Additionally, female pelvises widen during puberty through the influence of sex hormones. This wider pelvis requires the femur to angle toward the knees. This angle towards the knee is referred to as the Q angle. The average Q angle for men is 14 degrees and the average for women is 17 degrees. Steps can be taken to reduce this Q angle, such as using orthotics. The relatively wider female hip and widened Q angle may lead to an increased likelihood of ACL tears in women. ACL, muscular stiffness, and strength
During puberty, sex hormones also affect the remodeled shape of soft tissues throughout the body. The tissue remodeling results in female ACLs that are smaller and will fail (i.e. tear) at lower loading forces, and differences in ligament and muscular stiffness between men and women. Womens knees are less stiff than mens during muscle activation.