FLAVAMINE is a diterpenoid alkaloid isolated from the roots of Aconitum fiavum.

Acetergamine is a derivative of ergoline, it is an oxytocic agent. Acetergamine is alpha-1 blocker and vasodilator. It has been investigated as a treatment for cerebellar ataxia.

Turofexorate Isopropyl (XL335) is a potent, selective, and orally bioavailable FXR agonist. Binds to the ligand-binding domain (LBD) of human FXR. Turofexorate Isopropyl resides in a predominately hydrophobic pocket with only a few polar atoms making contact with WAY-362450. Turofexorate Isopropyl promotes transcription of the human BSEP, human SHP, and mouse IBABP genes utilizing reporter constructs with EC50 of 17, 230, and 33 nM, respectively in promoter assays. Turofexorate Isopropyl had been in phase I clinical trials for the treatment of hyperlipidemia. This compound was originally discovered by Exelixis Pharmaceuticals, then licensed to Wyeth (now a wholly-owned subsidiary of Pfizer). However, the studies were discontinued.

Lersivirine (UK-453,061) is a novel second-generation non-nucleoside reverse transcriptase inhibitor (NNRTI). It binds reverse transcriptase in a distinct way leading to a unique resistance profile. Lersivirine is a second-line NNRTI, which was investigated in a Phase IIb clinical trial. Lersivirine has shown encouraging virologic efficacy in a Phase IIa monotherapy study in NNRTI-naive patients. In a Phase IIb clinical trial in ART naive patients, clinical efficacy of lersivirine was compared with efavirenz, each administered together with tenofovir disoproxil fumarate/emtricitabine. After 48 weeks, lersivirine exhibited a slightly lower virologic response but similar immunologic efficacy. However, the trial was not powered for formal hypothesis testing of noninferiority of lersivirine. The development of lersivirine was recently stopped because the developing company determined that the compound would not provide an improvement over existing NNRTIs.

Nabitan is a synthetic cannabinoid analog of dronabinol with antiemetic and analgesic effects. Nabitan is not currently used in medicine as dronabinol or nabilone are felt to be more useful for most conditions, however, it is sometimes used in research into the potential therapeutic applications of cannabinoids.

Methyldesorphine is a synthetic narcotic analgesic derived from morphine. It has no medicinal value in the US. This compound is listed as a Schedule I Narcotic controlled substance under the Controlled Substances Act 1970.

Suronacrine (also known as HP128) is a tetrahydroacridinol derivative patented by Hoechst-Roussel Pharmaceuticals, Inc for the treatment of various memory dysfunctions characterized by decreased cholinergic function. The activity ofHP128 is attributable to its inhibition of both norepinephrine uptake and cholinesterase enzyme activity. Suronacrine has enhanced memory in animals with combined cholinergic and adrenergic lesions. In preclinical models, Suronacrine blocks responses to nerve stimulation and to carbachol, but increased responses to acetylcholine. Extracellular recording of nerve terminal currents from triangularis sterni preparations revealed that Suronacrine had a selective blocking action on the waveform associated with K+ currents.

Adamantyl is adamantly derivative patented by pharmaceutical company Scherico Ltd. as spasmolytic for treatment spasms associated with Parkinson's disease.

Camobucol is a novel, orally active, phenolic antioxidant and anti-inflammatory compound with antirheumatic properties. Camobucol exhibited potent antioxidant activity toward lipid peroxides in vitro and displayed enhanced cellular uptake relative to a structurally related drug, probucol. This resulted in potent inhibition of cellular levels of reactive oxygen species in multiple cell types. Camobucol selectively inhibited tumor necrosis factor (TNF)-alpha-inducible levels of the redox-sensitive genes, vascular cell adhesion molecule-1 and monocyte chemoattractant protein-1, with less inhibition of E-selectin, and no effect on intracellular adhesion molecule-1 expression in endothelial cells. In addition, Camobucol inhibited cytokine-induced levels of monocyte chemoattractant protein-1, interleukin (IL)-6, and IL-8 from endothelial cells and human fibroblast-like synoviocytes as well as lipopolysaccharide-induced release of TNF-alpha, IL-1beta, and IL-6 from human peripheral blood mononuclear cells. Camobucol did not inhibit TNF-alpha-induced nuclear translocation of nuclear factor of the kappa-enhancer in B cells (NF-kappaB), suggesting that the mechanism of action is independent of this redox-sensitive transcription factor.