Quinupristin is an antibiotic compound and a semisynthetic derivative of pristinamycin Ia. Quinupristin is a combination of three peptide macrolactones. Quinupristin is used in combination with dalfopristin, another antibiotic, under the trade name Synercid. Synercid is indicated for treatment of complicated skin and skin structure infections caused by methicillin-susceptible Staphylococcus aureus or Streptococcus pyogenes. The mechanism of action of quinupristin is inhibition of the late phase of protein synthesis in the bacterial ribosome. Quinupristin binds to 23S rRNA within the 50S ribosomal subunit and prevents elongation of the polypeptide as well as causing incomplete chains to be released. Adverse reactions to Synercid include inflammation at infusion site, rash, nausea, vomiting and others.

Gatifloxacin is a recently developed antibacterial agent differing from earlier fluoroquinolones by the presence of a methoxy group at the C-8 position. The presence of the methoxy group has conferred improved antibacterial activity against both Gram-positive and Gram-negative organisms, making gatifloxacin a broad-spectrum antimicrobial agent applicable in many clinical settings. Gatifloxacin is sold under the brand Zymar and is indicated for the treatment of bacterial conjunctivitis caused by susceptible strains of the following organisms: Aerobic Gram-Positive Bacteria: Cornyebacterium propinquum, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus mitis, Streptococcus pneumoniae and Aerobic Gram-Negative Bacteria: Haemophilus influenza. The antibacterial action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. In addition, Gatifloxacin inhibits bacterial topoisomerase IV. This enzyme is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division. The mechanism of action of fluoroquinolones including gatifloxacin is different from that of aminoglycoside, macrolide, and tetracycline antibiotics. Therefore, gatifloxacin may be active against pathogens that are resistant to these antibiotics and these antibiotics may be active against pathogens that are resistant to gatifloxacin. There is no cross-resistance between gatifloxacin and the aforementioned classes of antibiotics. Cross-resistance has been observed between systemic gatifloxacin and some other fluoroquinolones.

NEO 212 is novel DNA alkylating agent exhibiting superior activity against breast cancer cells in vitro and intracranial triple-negative tumor growth in vivo. NEO212 is a conjugate of temozolomide (TMZ,) with the natural product perillyl alcohol (POH). NEO 212 causes DNA damage and cell death much more efficiently than TMZ because linkage with POH increased it's biological half-life and thus provided greater opportunity for placement of cytotoxic DNA lesions.

Bexarotene (Targretin) is an antineoplastic agent indicated by the FDA for Cutaneous T cell lymphoma. It has been used off-label for lung cancer, breast cancer, and Kaposi's sarcoma. Bexarotene is a member of a subclass of retinoids that selectively activate retinoid X receptors (RXRs). These retinoid receptors have biologic activity distinct from that of retinoic acid receptors (RARs). Bexarotene selectively binds and activates retinoid X receptor subtypes (RXRa, RXRb, RXRg). RXRs can form heterodimers with various receptor partners such as retinoic acid receptors (RARs), vitamin D receptor, thyroid receptor, and peroxisome proliferator activator receptors (PPARs). Once activated, these receptors function as transcription factors that regulate the expression of genes that control cellular differentiation and proliferation. Bexarotene inhibits the growth in vitro of some tumor cell lines of hematopoietic and squamous cell origin. It also induces tumor regression in vivo in some animal models. The exact mechanism of action of bexarotene in the treatment of cutaneous T-cell lymphoma (CTCL) is unknown.

Thalidomide is an immunomodulatory agent with a spectrum of activity that is not fully characterized. Thalidomide is racemic — it contains both left and right-handed isomers in equal amounts: one enantiomer is effective against morning sickness, and the other is teratogenic. The enantiomers are converted to each other in vivo. That is, if a human is given D-thalidomide or L-thalidomide, both isomers can be found in the serum. Hence, administering only one enantiomer will not prevent the teratogenic effect in humans. In patients with erythema nodosum leprosum (ENL) the mechanism of action is not fully understood. Available data from in vitro studies and preliminary clinical trials suggest that the immunologic effects of this compound can vary substantially under different conditions, but may be related to suppression of excessive tumor necrosis factor-alpha (TNF-a) production and down-modulation of selected cell surface adhesion molecules involved in leukocyte migration. For example, administration of thalidomide has been reported to decrease circulating levels of TNF-a in patients with ENL, however, it has also been shown to increase plasma TNF-a levels in HIV-seropositive patients. As a cancer treatment, the drug may act as a VEGF inhibitor. Thalidomide is used for the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum (ENL). Also for use as maintenance therapy for prevention and suppression of the cutaneous manifestations of ENL recurrence. Thalidomide is sold under the brand name Immunoprin, among others.

Telmisartan is an orally active nonpeptide angiotensin II antagonist that acts on the AT1 receptor subtype. It was discovered by Boehringer Ingelheim and launched in 1999 as Micardis. It has the highest affinity for the AT1 receptor among commercially available ARBS and has minimal affinity for the AT2 receptor. New studies suggest that telmisartan may also have PPARγ agonistic properties that could potentially confer beneficial metabolic effects, as PPARγ is a nuclear receptor that regulates specific gene transcription, and whose target genes are involved in the regulation of glucose and lipid metabolism, as well as anti-inflammatory responses. This observation is currently being explored in clinical trials. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan works by blocking the vasoconstrictor and aldosterone secretory effects of angiotensin II. Telmisartan interferes with the binding of angiotensin II to the angiotensin II AT1-receptor by binding reversibly and selectively to the receptors in vascular smooth muscle and the adrenal gland. As angiotensin II is a vasoconstrictor, which also stimulates the synthesis and release of aldosterone, blockage of its effects results in decreases in systemic vascular resistance. Telmisartan does not inhibit the angiotensin converting enzyme, other hormone receptors, or ion channels. Studies also suggest that telmisartan is a partial agonist of PPARγ, which is an established target for antidiabetic drugs. This suggests that telmisartan can improve carbohydrate and lipid metabolism, as well as control insulin resistance without causing the side effects that are associated with full PPARγ activators. Used alone or in combination with other classes of antihypertensives for the treatment of hypertension. Telmisartan is used in the treatment of diabetic nephropathy in hypertensive patients with type 2 diabetes mellitus, as well as the treatment of congestive heart failure (only in patients who cannot tolerate ACE inhibitors).

Montelukast (SINGULAIR®) is a selective and orally active leukotriene D4 (LTD4) receptor antagonist that inhibits the cysteinyl leukotriene CysLT1 receptor. It is indicated for the prophylaxis and chronic treatment of asthma, for prevention of exercise-induced bronchoconstriction, and for the relief of symptoms of seasonal allergic rhinitis. LTD4 is a product of arachidonic acid metabolism and is released from various cells, including mast cells and eosinophils. This eicosanoid binds to CysLT1 receptor found in the human airway (including airway smooth muscle cells and airway macrophages) and on other pro-inflammatory cells (including eosinophils and certain myeloid stem cells). Cysteinyl leukotriene receptors (CysLTs) have been correlated with the pathophysiology of asthma and allergic rhinitis. In asthma, leukotriene-mediated effects include airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process. In allergic rhinitis, CysLTs are released from the nasal mucosa after allergen exposure during both earlyand late-phase reactions and are associated with symptoms of allergic rhinitis. Montelukast (SINGULAIR®) binds with high affinity and selectivity to the CysLT1 (in preference to other pharmacologically important airway receptors, such as the prostanoid, cholinergic, or beta-adrenergic receptor). It inhibits physiologic actions of LTD4 at the CysLT1 receptor without any agonist activity.

Candesartan is classified as an angiotensin II receptor type 1 antagonist. Candesartan is an orally active lipophilic drug and possesses rapid oral absorption. It causes a reduction in blood pressure and is used in the treatment of hypertension. It is also used in the treatment of congestive heart failure and given as prophylaxis to reduce the severity and duration of migraine. Candesartan cilexetil, a prodrug of Candesartan, is available in the market under the trade names Atacand, Amias. Candesartan cilexetil is rapidly converted to candesartan, its active metabolite, during absorption from the gastrointestinal tract. Candesartan confers blood pressure lowering effects by antagonizing the hypertensive effects of angiotensin II via the RAAS (renin–angiotensin–aldosterone system). RAAS is a homeostatic mechanism for regulating hemodynamics, water, and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from granular cells of the juxtaglomerular apparatus in the kidneys. Renin cleaves circulating angiotensinogen to angiotensin I, which is cleaved by angiotensin converting enzyme (ACE) to angiotensin II. Angiotensin II increases blood pressure by increasing total peripheral resistance, increasing sodium and water reabsorption in the kidneys via aldosterone secretion, and altering the cardiovascular structure. Angiotensin II binds to two receptors: type-1 angiotensin II receptor (AT1) and type-2 angiotensin II receptor (AT2). Candesartan selectively blocks the binding of angiotensin II to AT1 in many tissues including vascular smooth muscle and the adrenal glands. This inhibits the AT1-mediated vasoconstrictive and aldosterone-secreting effects of angiotensin II and results in an overall decrease in blood pressure. Candesartan is greater than 10,000 times more selective for AT1 than AT2.

Risedronic acid is a pyridinyl bisphosphonate that inhibits osteoclast-mediated bone resorption and modulates bone metabolism. The action of risedronate on bone tissue is based partly on its affinity for hydroxyapatite, which is part of the mineral matrix of bone. Risedronate also targets farnesyl pyrophosphate (FPP) synthase. It is FDA approved for the treatment of postmenopausal osteoporosis, osteoporosis in men, glucocorticoid-induced osteoporosis and Paget’s disease. Calcium, antacids, or oral medications containing divalent cations interfere with the absorption of Risedronic acid. Common adverse reactions include rash, abdominal pain, constipation, diarrhea, indigestion, nausea, backache, urinary tract infectious disease and influenza-like illness.