Esomeprazole strontium is a proton pump inhibitor. It suppresses gastric acid secretion by specific inhibition H+/K+ ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. The drug is indicated for the treatment of gastroesophageal reflux disease, reduction the risk of NSAID-associated gastric ulcer, eradication of H.pylori, and pathological hypersecretory conditions.

Corifungin refers to the sodium salt of amphotericin B. Although amphotericin B has become the primary drug of choice for treating primary amoebic meningoencephalitis, its use is associated with multiple side effects, including use-limiting renal toxicity. Initial reports for the in vivo efficacy of corifungin in a mouse model of primary amoebic meningoencephalitis showed activity superior to that of amphotericin B at equivalent dosing. Chemically, corifungin is the sodium salt of amphotericin B with excellent aqueous solubility. The increased solubility of corifungin is likely to account for the described increase in activity. Acea Biotech is developing corifungin for the treatment of fungal infections and amebic diseases. Acea has completed of host of animal studies on corifungin setting the stage to take the drug into the clinic. U.S. FDA has approved orphan drug status for corifungin for the treatment of primary amebic meningoencephalitis.

Boronophenylalanine B-10 (also known as BPA), a boron delivery agent, is used in boron-neutron capture therapy (BNCT) for metastatic melanomas and other tumors. BNCT is a therapeutic modality for malignant tumors using the nuclear capture and fission reactions that occur when boron-10 (10B) is irradiated with neutron beams. This reaction, in theory, only kills 10B-containing cells because the destructive effect of the alpha particles and lithium nuclei, which are produced by the reaction, is limited to the immediate vicinity of the reaction, approximately one cell diameter. Boronophenylalanine is localized to cells through transporter-mediated mechanisms. Aromatic amino acid transporters, ATB0,+, as well as LAT1 contribute significantly to the tumor accumulation of BPA at clinical dose.

Senexin B is a selective CDK8/CDK19 inhibitor developed by Senex Biotechnology Inc. Senexin B is an ATP pocket binder, with very high target selectivity as indicated by kinome profiling. CDK8/19 inhibition produces chemopotentiating, chemopreventive and anti-metastatic effects in different types of cancer.

AMPHOTERICIN B CHOLESTERYL SULFATE COMPLEX (AMPHOTEC) is an antifungal medicine. AMPHOTEC® is a sterile, pyrogen-free, lyophilized powder for reconstitution and intravenous (IV) administration. AMPHOTEC consists of a 1:1 (molar ratio) complex of amphotericin B and cholesteryl sulfate. AMPHOTEC is indicated for the treatment of invasive aspergillosis in patients where renal impairment or unacceptable toxicity precludes the use of amphotericin B deoxycholate in effective doses, and in patients with invasive aspergillosis where prior amphotericin B deoxycholate therapy has failed. The active ingredient of AMPHOTEC, amphotericin B, is a polyene antibiotic that acts by binding to sterols (primarily ergosterol) in cell membranes of sensitive fungi, with subsequent leakage of intracellular contents and cell death due to changes in membrane permeability. Amphotericin B also binds to the sterols (primarily cholesterol) in mammalian cell membranes, which is believed to account for its toxicity in animals and humans. AMPHOTEC is active against Aspergillus spp (A. fumigatus, A. flavus), Candida spp (C. albicans, C. krusei, C. parapsilosis, C. tropicalis), Cryptococcus neoformans, and Blastomyces dermatitidis. Active against most fungi with the notable exceptions of Candida lusitaniae, Trichosporon beigelii, Aspergillus terreus (some isolates), Pseudallescheria boydii, Malassezia furfur and Fusarium spp. The lipid formulations are designed to reduce binding of amphotericin to mammalian cell membranes, therefore reducing toxicities.

Friulimicin B (or friulimicin) is a naturally occurring antibiotic produced by a microorganism Actinoplanes friuliensis. This drug is active against a broad spectrum of gram-positive multi drug resistant, invasive pathogens. Friulimicin B participated in phase I clinical trials provided by MerLion Pharmaceuticals for the treatment of nosocomial infections. However, information about the further development of this drug is not available.

Borocaptate sodium B10 (also known as sodium borocaptate), a boron compound for use in boron neutron capture therapy. After parenteral administration, sodium borocaptate accumulates preferentially in tumor cells. When exposed to neutron irradiation, borocaptate absorbs neutrons and self-destructs releasing short-range alpha radiation and 'recoil' lithium in tumor cells, resulting in alpha radiation-induced tumor cell death. This highly selective, localized radio targeting of tumor cells, known as boron neutron capture therapy, spares adjacent normal tissues. Borocaptate sodium B10 was involved in phase I clinical trial in treating patients with glioblastoma multiforme removed during surgery to study the side effects. In addition, this compound participated in phase I clinical trials in tissues of patients with primary, metastatic, or recurrent thyroid cancer, head and neck cancer, or liver metastases from colorectal cancer to study the side effects. Besides, borocaptate sodium B10 was involved in phase-I clinical trials for Glioma in the European Union, however, this study was discontinued.

Latrunculin B originates from Latrunculia (now Negombata) magnifica, a sponge from the Red Sea. Latrunculin B inhibits the assembly of actin microfilaments by 1:1 molecular binding of free actin monomers in the cell cytoplasm. It may be a potential therapeutic agent for glaucoma. Latrunculin B induced destabilization of the actin microfilament and apoptosis in a dose-dependent manner, as demonstrated by morphological changes and nuclear condensation in the PC3M cells. In addition, it resulted in an increase in the levels of gamma-H2AX recruitment, implicating the induction of DNA damage, including double-strand breaks. Induction of Bax, with little effect on Bcl-2 expression, indicated that actin disruption causes apoptosis through activation of Bax signaling in PC3M cells. This data might helps to develop the strategy for actin-based anticancer chemotherapy against highly metastatic prostate cancer.