Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Quercetin is a unique bioflavonoid that has been extensively studied by researchers over the past 30 years. Quercetin, the most abundant of the flavonoids (the name comes from the Latin –quercetum, meaning oak forest, quercus oak) consists of 3 rings and 5 hydroxyl groups. Quercetin is a member of the class of flavonoids called flavonoles and forms the backbone for many other flavonoids including the citrus flavonoids like rutin, hesperidins, Naringenin and tangeritin. It is widely distributed in the plant kingdom in rinds and barks. The best described property of Quercetin is its ability to act as antioxidant. Quercetin seems to be the most powerful flavonoids for protecting the body against reactive oxygen species, produced during the normal oxygen metabolism or are induced by exogenous damage [9, 10]. One of the most important mechanisms and the sequence of events by which free radicals interfere with the cellular functions seem to be the lipid peroxidation leading eventually the cell death. To protect this cellular death to happen from reactive oxygen species, living organisms have developed antioxidant line of defense systems [11]. These include enzymatic and non-enzymatic antioxidants that keep in check ROS/RNS level and repair oxidative cellular damage. The major enzymes, constituting the first line of defence, directly involved in the neutralization of ROS/RNS are: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) The second line of defence is represented by radical scavenging antioxidants such as vitamin C, vitamin A and plant phytochemicals including quercetin that inhibit the oxidation chain initiation and prevent chain propagation. This may also include the termination of a chain by the reaction of two radicals. The repair and de novo enzymes act as the third line of defence by repairing damage and reconstituting membranes. These include lipases, proteases, DNA repair enzymes and transferases. Quercetin is a specific quinone reductase 2 (QR2) inhibitor, an enzyme (along with the human QR1 homolog) which catalyzes metabolism of toxic quinolines. Inhibition of QR2 in plasmodium may potentially cause lethal oxidative stress. The inhibition of antioxidant activity in plasmodium may contribute to killing the malaria causing parasites.

Fumagillin, an antimicrobial compound first isolated in 1949 from the fungus Aspergillus fumigatusa, naturally occurring water-insoluble antibacterial agent developed by sanofi-aventis, is approved in France for the treatment of microsporidiosis. Fumagillin (Flisint, Sanofi-Aventis, Paris, France) has been approved in France since 2002 for the treatment of intestinal microsporidiosis due to E. bieneusi in patients with AIDS, and is also available through an expanded access program for patients without AIDS. It has not been approved, however, by the US Food and Drug Administration. The discovery of fumagillin, a MetAP-2 inhibitor, with potent antiangiogenic and antiproliferative activities promoted the development of fumagillin analogues as a novel class of anticancer agents. It has been the subject of research in cancer treatments by employing its angiogenesis inhibitory properties.

Amodiaquine is a medication used to treat malaria, including Plasmodium falciparum malaria when uncomplicated. The mechanism of plasmodicidal action of amodiaquine is not completely certain. Like other quinoline derivatives, it is thought to inhibit heme polymerase activity. This results in accumulation of free heme, which is toxic to the parasites. The drug binds the free heme preventing the parasite from converting it to a form less toxic. This drug-heme complex is toxic and disrupts membrane function. The side effects of amodiaquine are generally minor to moderate and are similar to those of chloroquine. Rarely liver problems or low blood cell levels may occur. When taken in excess headaches, trouble seeing, seizures, and cardiac arrest may occur. After oral administration amodiaquine hydrochloride is rapidly absorbed,and undergoes rapid and extensive metabolism to desethylamodiaquine which concentrates in red blood cells. It is likely that desethylamodiaquine, not amodiaquine, is responsible for most of the observed antimalarial activity, and that the toxic effects of amodiaquine after oral administration may in part be due to desethylamodiaquine.

Amodiaquine is a medication used to treat malaria, including Plasmodium falciparum malaria when uncomplicated. The mechanism of plasmodicidal action of amodiaquine is not completely certain. Like other quinoline derivatives, it is thought to inhibit heme polymerase activity. This results in accumulation of free heme, which is toxic to the parasites. The drug binds the free heme preventing the parasite from converting it to a form less toxic. This drug-heme complex is toxic and disrupts membrane function. The side effects of amodiaquine are generally minor to moderate and are similar to those of chloroquine. Rarely liver problems or low blood cell levels may occur. When taken in excess headaches, trouble seeing, seizures, and cardiac arrest may occur. After oral administration amodiaquine hydrochloride is rapidly absorbed,and undergoes rapid and extensive metabolism to desethylamodiaquine which concentrates in red blood cells. It is likely that desethylamodiaquine, not amodiaquine, is responsible for most of the observed antimalarial activity, and that the toxic effects of amodiaquine after oral administration may in part be due to desethylamodiaquine.

Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1, 1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.

Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1, 1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.

Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1, 1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.

Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1, 1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.