Monophosphothiamine is thiamine derivative used for the treatment of neuritis, polyneuritis, asthenic conditions (weakness), as an additional remedy for chronic blood circulation insufficiency, chronic gastritis accompanied by motor and secretory disorders functions of the stomach. Monophosphothiamine underwent metabolic phosphorylation to active metabolite thiamine pyrophosphate, that acts as a coenzyme in the different metabolic process.

Cilengitide is a cyclized Arg-Gly-Glu (RGD)-containing pentapeptide that selectively blocks activation of the αvβ3 and αvβ5 integrins. Its precursor was first synthesized in 1995 as c(RGDfV), and later modified by the incorporation of N-methyl Val c(RGDfMetV), generating the current form of the drug. Cilengitide displays subnanomolar antagonistic activity for αvβ3 and αvβ5, and is the first integrin antagonist evaluated in clinical phase I and II trials for treatment of glioblastoma and several other tumor types. Cilengitide-induced glioma cell death and inhibition of blood vessel formation may use different molecular mechanisms, including regulation of tumor hypoxia and activation of apoptotic pathways. Cilengitide inhibits cell signaling through FAK-Src-Akt and Erk mediated pathways in endothelial and tumor cells and attenuates the effect of VEGF stimulation on growth factor signaling. Cilengitide has shown encouraging activity in patients with glioblastoma as single agent, and in association with standard RT and temozolomide.

Cilengitide is a cyclized Arg-Gly-Glu (RGD)-containing pentapeptide that selectively blocks activation of the αvβ3 and αvβ5 integrins. Its precursor was first synthesized in 1995 as c(RGDfV), and later modified by the incorporation of N-methyl Val c(RGDfMetV), generating the current form of the drug. Cilengitide displays subnanomolar antagonistic activity for αvβ3 and αvβ5, and is the first integrin antagonist evaluated in clinical phase I and II trials for treatment of glioblastoma and several other tumor types. Cilengitide-induced glioma cell death and inhibition of blood vessel formation may use different molecular mechanisms, including regulation of tumor hypoxia and activation of apoptotic pathways. Cilengitide inhibits cell signaling through FAK-Src-Akt and Erk mediated pathways in endothelial and tumor cells and attenuates the effect of VEGF stimulation on growth factor signaling. Cilengitide has shown encouraging activity in patients with glioblastoma as single agent, and in association with standard RT and temozolomide.

m-Chlorophenylpiperazine (meta-chlorophenylpiperazine or mCPP) is a psychoactive substance, which is illegal in many countries but can be found on the black market. It induces endocrine, neurological and psychiatric effects. mCPP is a partial agonist at the 5-HT2C receptor but antagonized the 5-HT2B and 5-HT3 receptors. mCPP is also an active metabolite of the drug trazodone, which is used as an effective antidepressant drug with a broad therapeutic spectrum, including anxiolytic efficacy. It is known, that mCPP induces migraine attacks and that the decrease of food intake induced by the mCPP depends on its ability to act as a serotonin agonist is a brain.

Glesatinib (MGCD265) is an orally bioavailable, small-molecule, multitargeted tyrosine kinase inhibitor with potential antineoplastic activity. Glesatinib binds to and inhibits the phosphorylation of several receptor tyrosine kinases (RTKs), including the c-Met receptor (hepatocyte growth factor receptor); the Tek/Tie-2 receptor; vascular endothelial growth factor receptor (VEGFR) types 1, 2, and 3; and the macrophage-stimulating 1 receptor (MST1R or RON). Inhibition of these RTKs and their downstream signaling pathways may result in the inhibition of tumor angiogenesis and tumor cell proliferation in tumors overexpressing these RTKs. Studies in a gastric cancer xenograft model revealed that, in addition to the typically reported cellular activities, glesatinib in combination with erlotinib disrupted the glycolysis pathway, suggesting a novel mechanism of action for this drug. Glesatinib has been studied in a variety of advanced solid tumors including NSCLC, as a monotherapy and in combination with either docetaxel or erlotinib. In an ongoing phase 1 study in patients with MET positive or AXL-rearranged advanced solid tumors, glesatinib demonstrated preliminary single-agent activity, with all three patients with MET dysregulated NSCLC (two with METex14 alterations and one with increased GCN) showing significant tumor regression at the first assessment. A phase 2 study is currently recruiting patients with MET-dysregulated (mutated or amplified) advanced or metastatic NSCLC.

Chloracyzine is phenothiazine derivative with vasodilatory activity. Chloracyzine produced a decrease in myocardial oxygen consumption accompanied by a reduction in coronary blood flow preceded by transient coronary dilatation. Chloracyzine produced an insignificant increase in arterial pressure; heart rate increased slightly in the open-chest experiments but not in the isolated heart. It is suggested that reduced oxygen uptake after chloracyzine is realized through improved efficiency in the use of oxygen.

Cevipabulin is a synthetic, water-soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth.

Cevipabulin is a synthetic, water-soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth.

Atropine-N-oxide hydrochloride is an alkaloid of the belladonna plants. It is the major metabolite of atropine. It is a competitive nonselective antagonist at central and peripheral muscarinic acetylcholine receptors.