Aliskiren – the only direct renin inhibitor which is clinically used as an antihypertensive drug. Aliskiren is the first of a new class of antihypertensive agents. Aliskiren is a new renin inhibitor of a novel structural class that has recently been shown to be efficacious in hypertensive patients after once-daily oral dosing. In short-term studies, it was effective in lowering blood pressure either alone or in combination with valsartan and hydrochlorothiazide, and had a low incidence of serious adverse effects. It was approved by the Food and Drug Administration in 2007 for the use as a monotherapy or in combination with other antihypertensives. Aliskiren is marketed under the trade name Tekturna. Aliskiren effectively reduces functional plasma renin activity by binding to renin with high affinity, preventing it from converting angiotensinogen to angiotensin I. The inhibition of renin by aliskiren is associated with a reduction in circulating levels of angiotensin I and II, with a resultant increase in plasma renin concentration and inhibit activation of mitogen-activated protein kinases ERK1 (p44) and ERK2 (p42).

Desloratadine is an active, descarboethoxy metabolite of loratadine. It acts by selective inhibition of H1 histamine receptor and thus provides relief to patients with allergic rhinitis and chronic idiopathic urticaria. Desloratadine was approved by FDA and it is currently marketed under the name Clarinex (among the others).

Ketotifen is a cycloheptathiophene blocker of histamine H1 receptors and release of inflammatory mediators. It has been proposed for the treatment of asthma, rhinitis, skin allergies, and anaphylaxis. Ketotifen was developed in 1970 by Sandoz Pharmaceuticals of Switzerland. It is a benzocycloheptathiophene derivative and was initially marketed as an inhibitor of anaphylaxis. The pharmacodynamic properties of ketotifen are many, because it is an inhibitor of the release and/or activity of mast cell and basophil mediators, including histamine, neutrophil, and eosinophil chemotactic factors, arachidonic acid metabolites, prostaglandins, and leukotrienes. Properties of ketotifen which may contribute to its antiallergic activity and its ability to affect the underlying pathology of asthma include inhibition of the development of airway hyper-reactivity associated with activation of platelets by PAF (Platelet Activating Factor), inhibition of PAF-induced accumulation of eosinophils and platelets in the airways, suppression of the priming of eosinophils by human recombinant cytokines and antagonism of bronchoconstriction due to leukotrienes. Ketotifen is marketed under many brand names worldwide. Ketotifen inhibits the release of mediators from mast cells involved in hypersensitivity reactions. Decreased chemotaxis and activation of eosinophils have also been demonstrated. Ketotifen also inhibits cAMP phosphodiesterase.

Codeine is an opiate used to manage mild to moderate pain severe enough to require an opioid. Codeine is a selective agonist for the mu opioid receptor and has an affinity to delta and kappa-opioid receptors. In some countries, this drug is regulated under various narcotic control laws, because its chronic use can cause physical dependence. In others, it is available without a medical prescription in combination with paracetamol.

Monomethyl Auristatin E (MMAE) is an antimitotic agent which inhibits cell division by blocking the polymerization of tubulin. Monomethyl Auristatin E is the synthetic analog of the antineoplastic natural product Dolastatin 10, cannot be used as a drug itself. Monomethyl Auristatin E is commonly conjugated with monoclonal antibodies directed at antigens specific to cancer cells for tumor-directed cytotoxicity. MMAE is typically coupled to the antibody via a protease-cleavable linker, allowing separation of the drug from the antibody following intracellular localization. When coupled to cAC10, Monomethyl Auristatin E shows selective cytotoxicity in CD30+ cells and induces G2/M-phase growth arrest and cell death through the induction of apoptosis. When coupled to the anti-CD79b antibody, anti–CD79b-vcMMAE has very potent and broad activity across a large panel of NHL cell lines in vitro. When coupled to the anti-HER2 antibody, pertuzumab-vc-MMAE can also be effectively internalized and potently kill HER2 over-expressing tumor cells. In the Karpas 299 ALCL model, cAC10-vcMMAE induces complete, durable tumor regression, while free MMAE doesn’t produce detectable antitumor activity. In mouse xenograft models of NHL, anti–CD79b-vcMMAE strikingly results in sustained complete tumor remission.