Thursday, 25 August 2016

MyFol 400-RG Pharmaceutica





Tariq Haider RG Pharmaceutica  made the medicine L-Methylfolate with the name of MyFol 400 Folate is a general term that refers to compounds not only structurally but also with activity similar to that of folic acid. Folic acid (2-amino-4-hydroxy-6-metilenoaminobenzoil-glutamic acid), also known as pteroylglutamic acid, vitamin B9 and vitamin F, is naturally present in foods, generally, in reduced form, such as polyglutamates derivatives with 2 to 7 glutamic acid residues known as folates. To be used by our body folic acid must be converted to its active form - 5-MTHF.
High levels of homocysteine ​​involve the cardiovascular system disorders including thrombosis, stroke, atherosclerosis and myocardial infarction. 5-MTHF in addition to reducing the levels of homocysteine ​​in the blood, also enhances blood flow in peripheral arteries, thus increasing nitric oxide (NO) in the vascular endothelium. Most risk factors for atherosclerosis are associated with deficiency in vasodilation due to insufficient production of NO (chronic exposure of vascular endothelial cells to homocysteine ​​compromises the proper production of NO), this leads to endothelial injury and the onset of atherosclerosis, including increased adhesion of monocytes and platelets, increased smooth muscle proliferation and thrombus formation. 5-MTHF enhances synthesis.

 Reduction of homocysteine ​​plasma levels, thereby increasing the availability of endothelial cofactors such as tetrahydrobiopterin; 

RENEGYRG-RG Pharmaceutical



RG Pharmaceutical-RENEGY is a solution for parenteral (intravenous) formed by a highly stable complex ferric iron (Fe3 +) covered by a structure formed by a high molecular weight carbohydrate (carboxymaltose). Due to the high stability of the complex, the carboxymaltose RENEGY  does not release ionic iron directly into the bloodstream, preventing it from causing cell damage due to oxidative stress in
the body.
After intravenous administration of RENEGY, and incorporation into the plasma, this progressively penetrates in the reticuloendothelial system (RES) from the intravascular compartment, to the resident macrophages of the liver, spleen and bone marrow being phagocytized and deposited in intracellular lysosomes where ferric iron (Fe 3+) is reduced to its ferrous form (Fe 2+) according to the body's requirements. 
Once the ferric iron (Fe 3+) is reduced to ferrous form (Fe 2+) inside the lysosome, it is captured by the divalent metal transporter (by its acronym T1DM), which are in the lysosome membrane and release the iron in the macrophage cytoplasm labile form. And in the macrophage cytoplasm, iron can be grasped by ferroportin for transportation outside the macrophage or ferritin for storage. This process is regulated largely by hepcidin, which allow, in case of decrease in plasma iron concentration, binding of the ferrous iron to ferroportin to be transported through the macrophage membrane and released to the outside.