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Adding PDE5 inhibitors to SSRI drugs (e.g. paroxetine) for the treatment of premature ejaculation could result in better ejaculatory control according to recent studies. [11] Possible mechanism is based on nitric oxide (NO)/cGMP transduction system as a central and peripheral mediator of inhibitory non-adrenergic, non-cholinergic nitrergic ...
Because of the difference in FAS expression between normal cells and cancer cells, orlistat selectively targets tumor cells. Due to this FAS is a potential drug target in cancer therapy. [34] [37] Orlistat works locally in the intestines as a lipase inhibitor, and therefore suffers from several limitations in its development as a systemic drug.
When the enzyme adenosine deaminase is deficient in the body, the result is a toxic build-up of metabolites that impair lymphocyte development and function. [9] Many ADA deficient children with SCID have been treated with the polyethylene glycol-conjugated adenosine deaminase (PEG-ADA) enzyme.
Dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitors) are enzyme inhibitors that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4). They are used in the treatment of type 2 diabetes mellitus. Inhibition of the DPP-4 enzyme prolongs and enhances the activity of incretins that play an important role in insulin secretion and blood glucose control ...
This knowledge paved the way for the development of selective inhibitors. [6] HIV-2 carries a slightly lower risk of transmission than HIV-1 and infection tends to progress more slowly to AIDS. [7] In common usage HIV usually implies HIV-1. [8] HIV-1 protease is one of the best known aspartic proteases, and an attractive target for the ...
These drugs have emerged as the treatment of choice for acid-related diseases, including gastroesophageal reflux disease (GERD) and peptic ulcer disease. PPIs also can bind to other types of proton pumps such as those that occur in cancer cells and are finding applications in the reduction of cancer cell acid efflux and reduction of ...
The two enzymes were renamed COX-1, referring to the original enzyme and COX-2. [5] Building on those results, scientists started focusing on selective COX-2 inhibitors. Enormous effort was spent on the development of NSAIDs between the 1960s and 1980 so there were numerous pharmacophores to test when COX-2 was discovered.
[1] [2] [3] Many chemotherapy drugs for cancer lack tumour specificity and the doses required to reach therapeutic levels in the tumour are often toxic to other tissues. DEPT strategies are an experimental method of reducing the systemic toxicity of a drug, by achieving high levels of the active drug only at the desired site.