Bevirimat (3-O-(3',3'-dimethylsuccinyl) betulinic acid or MPC-4326 or PA-457) potently inhibits replication of both WT and drug-resistant HIV-1 isolates and demonstrate that the compound acts by disrupting a late step in Gag processing involving conversion of the capsid precursor (p25) to mature capsid protein (p24). Bevirimat inhibits replication of both wild-type and drug-resistant HIV-1 isolates in vitro, achieving similar 50% inhibitory concentration values with both categories. Serial drug passage studies have identified six single amino acid substitutions that independently confer bevirimat resistance. These resistance mutations occur at or near the CA-SP1 cleavage site, which is not a known target for resistance to other antiretroviral drugs. Bevirimat has been in phase 2 trial for the treatment of HIV infections. Bevirimat has demonstrated a consistent pharmacokinetic profile in healthy volunteers and HIV-infected patients. The demonstration of an antiviral effect following a single oral dose of bevirimat validates maturation inhibition as a potential target for antiretroviral therapeutics in humans.

EQUOL, (-)- is the (S)-enantiomer of the naturally-occurring isoflavandiol estrogen, equol. EQUOL, (-)- (US-131), is a first-in-class, nonsteroidal, nonhormonal, small molecule (S-equol) that has higher selectivity toward estrogen receptor β (ERβ) than to estrogen receptor α (ERα). S-equol is the exclusive product of human intestinal bacterial synthesis from soy isoflavones. Two-Phase 1 studies have seen completed and published; AUS-131 was safe and well-tolerated in humans. A Phase 2a trial in menopausal women with vasomotor symptoms (VMS) has recently been completed (169 patients). A second Phase 2a trial in men with benign prostatic hyperplasia (BPH) is on track.

Balicatib is a potent cathepsine K inhibitor that was developed for the treatment of knee osteoarthritis. The development of Balicatib was terminated in phase II due to the occurrence of skin rashes and rarer incidences of morphea-like skin changes.

Furosemide is a non-antibiotic bacterial urease inhibitor that can be used in the control of H. pylori-associated gastroduodenal disease.

Atigliflozin (also known as AVE2268), a substituted glycopyranoside, is a selective inhibitor of sodium-dependent glucose transporter 2. This drug reached phase II clinical trials as a new antidiabetic drug for the treatment of type 2 diabetes but further development was discontinued.

Y-700 (Niraxostat or 1-[3-Cyano-4-(2,2-dimethylpropoxy)phenyl]-1H-pyrazole-4-carboxylic acid) is an inhibitor of xanthine oxidoreductase. Y-700 demonstrated high oral bioavailability being predominantly eliminated via the liver. It potently reduces serum uric acid levels. Y-700 was in clinical trials for the treatment of gout.

Proclonol is a cyclopropylmethanol derivative patented by Belgium pharmaceutical company Janssen Pharmaceutica N. V. as an arachnicide and fungicide. Tetranychus urticae in the adult stage on bean plants were killed within 3 days with a spray contg. 35 ppm. Proclonol, while all of the larval stage on strawberry leaves was killed by 62.5 ppm., and no eggs sprayed with 40 ppm. hatched. A suspension of 500 ppm. Proclonol used to dip strawberry leaves infested with Tarsonemus pallidus killed 96.2% of the mites.

SGI-1776 is a PIM-kinase inhibitor, developed by SuperGen Inc. SGI-1176 was tested in clinical trials against relapsed/refractory leukemias, prostate cancer and Non Hodgkin's Lymphoma, but the dose limiting toxicity of cardiac QTc prolongation was identified and clinical development of SGI-1776 was terminated.

Decominol is a bactericidal compound used in the cosmetic industry and developed by the French company Laboratoires Pharmascience. Bacteriostatic activity is claimed to be particularly significant in the case of gram-negative bacteria, especially Escherichia coli and Pseudomonas aeruginosa.

JNJ-26854165 (Serdemetan), a novel tryptamine derivative, was developed as an activator of p53, and its initially proposed mechanism of action involved preventing the association of HDM2 with the proteasome and thereby stabilizing HDM2 substrates such as p53. Consistent with this proposed mechanism, Serdemetan induced apoptosis in acute myeloid and lymphoid leukemia cell lines and in primary acute leukemia isolates. Serdemetan is currently being evaluated in Phase I clinical trials in patients with non-small cell lung cancer; prostate cancer; solid tumours.