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.

Efepristin (RPR 106972) is an oral streptogramin consisting of two synergistic components RPR 112808 (pristinamycin IB) and RPR 106950 (pristinamycin IIB). It demonstrated activity against Gram-positive microorganisms in vitro and in vivo, including those with multi-drug resistance. The streptogramins inhibit bacterial growth by disrupting the translation of mRNA into protein.

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.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mutagenic and carcinogenic heterocyclic amine formed during ordinary cooking, and is subsequently metabolically activated by cytochrome P4501A2 (CYP1A2) and N-acetyltransferase 2 (NAT2). PhIP has been used in trials studying the basic science of Pancreas Cancer.

Cytochalasin B is a cell-permeable alkaloid, isolated from a fungus Helminthosporium dematioideum. Cytochalasin B is an inhibitor of actin polymerization through binding to the fast-growing (barbed) end of F-actin filaments. Cytochalasin is used in studies of actin polymerization, cell division, and cell movement. The compound also inhibits glucose transporters GLUT1,3 and 4 and was investigated in a clinical trial to prevent restenosis after angioplasty surgery.