Sulfamethoxazole is a synthetic antibacterial drug,which is used in combination with trimethoprim (Bactrim, Septra) for the treatment or prevention of infections that are proven or strongly suspected to be caused by bacteria. Sulfamethoxazole acts by inhibiting folic acid synthesis via enzyme called dihydropteroate synthase.

Lumacaftor (VX-809) is an investigational drug developed by the Massachusetts-based pharmaceutical company Vertex for the treatment of patients who suffer from cystic fibrosis (CF) and have the F508del mutation in the CF transmembrane conductance regulator (CFTR). Currently, lumacaftor is approved by the U.S. FDA as a combined oral treatment for CF in combination with Kalydeco (ivacaftor). Lumacaftor is commercialized by Vertex under the brand name Orkambi, and Kalydeco was approved in the United States in 2012. The lumacaftor/Kalydeco combo was approved by the FDA in July 2015 for patients ages 12 and older, while the use of lumacaftor alone is still being studied by Vertex. The mechanism of action of lumacaftor is based on the interference with the F508 CFTR. The chronic disease is caused by a mutation in the gene that controls the salt transportation in the cells, resulting in thick, sticky mucus in the respiratory, digestive, and reproductive systems. To address that genetic defect, lumacaftor helps correct the mutated genes with a novel therapeutic approach. Both lumicaftor and kalydeco work by correcting the misfolded CFTR protein, the root cause of the F508del mutation, which led to the approval of the combined treatment by the FDA. However, while kalydeco alone is also approved by the FDA, the use of lumacftor alone has not yet been approved.

Ceritinib is a selective inhibitor of ALK1, a target found in metastatic non-small cell lung cancer (NSCLC). Ceritinib is approved by FDA and is indicated for the treatment of anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer. Ceritinib also targets insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1.

Oritavancin is an glycopeptide antibiotic with bactericidal activity effective in treating infections caused by Gram-positive organisms. It treats complicated skin and skin structure infections. This drug demonstrates similar activity to vancomycin, but it has stronger activity against Staphylococcus and Enterococcus. The pharmacokinetics and pharmacodynamics of oritavancin appear to be favourable and once-daily dosing is likely. The incidence of multi-drug resistant bacteria is increasing and explorations into additional treatment options are essential. Oritavancin is marketed under the brand name Orbactiv. Orbactiv is indicated for the treatment of adult patients with acute bacterial skin and skin structure infections caused or suspected to be caused by susceptible isolates of designated Gram-positive microorganisms. Oritavancin has the following mechanism of action: 1) Inhibition of the transglycosylation (polymerisation) step of cell wall biosynthesis by binding to the stem peptide of peptidoglycan precursors 2) Inhibition of the transpeptidation (crosslinking) step of cell wall biosynthesis by binding to the peptide bridging segments of the cell wall 3) Disruption of bacterial membrane integrity, leading to depolarisation, increased permeability and rapid cell death.

Regorafenib (trade name Stivarga) is an orally bioavailable small molecule with potential antiangiogenic and antineoplastic activities. Regorafenib binds to and inhibits vascular endothelial growth factor receptors (VEGFRs) 2 and 3, and Ret, Kit, PDGFR and Raf kinases, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation. VEGFRs are receptor tyrosine kinases that play important roles in tumor angiogenesis; the receptor tyrosine kinases RET, KIT, and PDGFR, and the serine/threonine-specific Raf kinase are involved in tumor cell signaling. In in vivo models, regorafenib demonstrated anti-angiogenic activity in a rat tumor model, and inhibition of tumor growth as well as anti-metastatic activity in several mouse xenograft models including some for human colorectal carcinoma. Since 2009 it was studied as a potential treatment option in multiple tumor types. Stivarga is approved by FDA to treat two different tumor types: metastatic colorectal cancer in patients who have been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an anti-VEGF therapy, and, if KRAS wild type, an anti-EGFR therapy (approved in 2012) and to treat patients with locally advanced, unresectable or metastatic gastrointestinal stromal tumor who have been previously treated with imatinib mesylate and sunitinib malate (approved in 2013).

Ivacaftor (trade names KALYDECO® (ivacaftor) and ORKAMBI® (lumacaftor/ivacaftor)) is a cystic fibrosis transmembrane conductance regulator potentiator indicated for the treatment of cystic fibrosis in patients age 6 years and older who have one of the following mutations in the CFTR gene: G551D, G1244E, G1349D, G178R, G551S, S1251N, S1255P, S549N, or S549R. One such defect G551D is characterized by a dysfunctional CFTR protein on the cell surface. Although the defective protein is trafficked to the correct area, the epithelial cell surface, while there it cannot transport chloride through the channel. Ivacaftor, a CFTR potentiator, improves the transport of chloride through the ion channel by binding to the channels directly to induce a non-conventional mode of gating which in turn increases the probability that the channel is open. Ivacaftor regulates fluid flow within cells and affects the components of sweat, digestive fluids, and mucus.

Voriconazole (vor-i-KON-a-zole, brand name Vfend, Pfizer) is a triazole antifungal medication. VFEND® (voriconazole) is available as film-coated tablets for oral administration, and as a lyophilized powder for solution for intravenous infusion. Voriconazole is a triazole antifungal agent indicated for use in the treatment of fungal infections including invasive aspergillosis, esophageal candidiasis, and serious fungal infections caused by Scedosporium apiospermum (asexual form of Pseudallescheria boydii) and Fusarium spp. including Fusarium solani. Fungal plasma membranes are similar to mammalian plasma membranes, differing in having the nonpolar sterol ergosterol, rather than cholesterol, as the principal sterol. Membrane sterols such as ergosterol provide structure, modulation of membrane fluidity, and possibly control of some physiologic events. Voriconazole effects the formation of the fungal plasma membrane by indirectly inhibiting the biosynthesis of ergosterol. This results in plasma membrane permeability changes and inhibition of growth. The primary mode of action of voriconazole is the inhibition of fungal cytochrome P-450-mediated 14 alpha-lanosterol demethylation, an essential step in fungal ergosterol biosynthesis. The accumulation of 14 alpha-methyl sterols correlates with the subsequent loss of ergosterol in the fungal cell wall and may be responsible for the antifungal activity of voriconazole. Voriconazole has been shown to be more selective for fungal cytochrome P-450 enzymes than for various mammalian cytochrome P-450 enzyme systems. The most common side effects associated with voriconazole include transient visual disturbances, fever, rash, vomiting, nausea, diarrhea, headache, sepsis, peripheral edema, abdominal pain, and respiratory disorder. Unlike most adverse effects, which are similar to other azole antifungal agents, visual disturbances (such as blurred vision or increased sensitivity to light) are unique to voriconazole. Though rare, there have been cases of serious hepatic reactions during treatment with voriconazole (a class effect of azole antifungal agents). Liver function tests should be evaluated at the start of and during the course of therapy. Voriconazole is phototoxic. It has been associated with an increased risk of squamous-cell carcinoma of the skin

Efavirenz (brand names Sustiva® and Stocrin®) is a non-nucleoside reverse transcriptase inhibitor (NNRTI) and is used as part of highly active antiretroviral therapy (HAART) for the treatment of a human immunodeficiency virus (HIV) type 1. For HIV infection that has not previously been treated, efavirenz and lamivudine in combination with zidovudine or tenofovir is the preferred NNRTI-based regimen. Efavirenz is also used in combination with other antiretroviral agents as part of an expanded postexposure prophylaxis regimen to prevent HIV transmission for those exposed to materials associated with a high risk for HIV transmission.

Trimethoprim (TMP) is an antibiotic is used for the treatment of initial episodes of uncomplicated urinary tract infections due to susceptible strains of the following organisms: Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae, Enterobacter species, and coagulase-negative Staphylococcus species, including S. saprophyticus. Cultures and susceptibility tests should be performed to determine the susceptibility of the bacteria to trimethoprim. Therapy may be initiated prior to obtaining the results of these tests. Trimethoprim is rapidly absorbed following oral administration. It exists in the blood as unbound, protein-bound, and metabolized forms. Ten to twenty percent of trimethoprim is metabolized, primarily in the liver; the remainder is excreted unchanged in the urine. The principal metabolites of trimethoprim are the 1- and 3-oxides and the 3'- and 4'-hydroxy derivatives. The free form is considered to be the therapeutically active form. Approximately 44% of trimethoprim is bound to plasma proteins. Trimethoprim blocks the production of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting the required enzyme, dihydrofolate reductase. This binding is very much stronger for the bacterial enzyme than for the corresponding mammalian enzyme