Methyl salicylate (or methyl 2-hydroxybenzoate), also known as wintergreen oil, is a natural product and is present in white wine, tea, porcini mushroom Boletus edulis, Bourbon vanilla, clary sage, red sage and fruits including cherry, apple, raspberry, papaya and plum. Methyl salicylate is topically used in combination with methanol and under brand name SALONPAS to temporarily relieves mild to moderate aches and pains of muscles and joints associated with: strains, sprains, simple backache, arthritis, bruises. The precise mechanism of action of methyl salicylate is not known, but there is suggested, that it cause dilation of the capillaries thereby increasing blood flow to the area.

Methyl salicylate (or methyl 2-hydroxybenzoate), also known as wintergreen oil, is a natural product and is present in white wine, tea, porcini mushroom Boletus edulis, Bourbon vanilla, clary sage, red sage and fruits including cherry, apple, raspberry, papaya and plum. Methyl salicylate is topically used in combination with methanol and under brand name SALONPAS to temporarily relieves mild to moderate aches and pains of muscles and joints associated with: strains, sprains, simple backache, arthritis, bruises. The precise mechanism of action of methyl salicylate is not known, but there is suggested, that it cause dilation of the capillaries thereby increasing blood flow to the area.

PX-102 is a methoxyphenylcyclopropane derivative patented by Phenex Pharmaceuticals AG as Farnesoid X receptor agonists useful in the treatment and prophylaxis of FXR-mediated diseases. The Farnesoid X Receptor (FXR) is a bile acid receptor which when activated by Px-102 has a profound positive impact on cholesterol, triglyceride and glucose metabolism in liver and intestine. In preclinical studies, Px-102 potently reduces intestinal uptake of neutral lipids and cholesterol and at the same time enhances the excretion of these lipid species. In addition, Px-102 improves hepatic insulin sensitivity and shows massive hepatoprotective effects in animal models of liver cirrhosis or fibrosis. Phenex Pharmaceuticals completes a phase I trial in Healthy volunteers in Germany in 2012 and no further development report has been published.

1,1-DIETHYL-4-PHENYLHOMOPIPERAZINIUM (ASM-024), a small synthetic molecule in clinical stage development, has shown activity at the level of nicotinic receptors and possibly at the muscarinic level and presents anti-inflammatory and bronchodilator properties. Aerosolized ASM-024 reduces airway resistance in mice and promotes in-vitro relaxation of tracheal and bronchial preparations from animal and human tissues. ASM-024 increased in vitro relaxation response to maximally effective concentration of short-acting beta-2 agonists in dog and human bronchi. ASM-024 is able to activate the α7 nAChR channel opening in the presence of the positive allosteric modulator (PNU-120596), indicating that ASM-024 behaves as a ‘silent agonist’ that places the receptor in a desensitized state. Compounds with similar properties have been shown to induce signal transduction pathways independently of ion channel activation. ASM-024 has demonstrated an antagonist effect on ACH-evoked activation at the M1, M2 and M3 muscarinic receptors expressed in Xenopus oocytes. A comprehensive nonclinical safety program was conducted with ASM-024 including pharmacokinetic and metabolism studies, safety pharmacology studies, toxicology and genotoxicity studies. In all, seven clinical studies were completed to evaluate the safety, tolerability and clinical activity of ASM-024. Three Phase I and four Phase II clinical trials were conducted on healthy subjects and patients with mild allergic asthma, stable moderate asthma and subjects with COPD. Altogether, ASM-024 has been safely administered to more than 200 subjects via the oral and inhalation delivery, i.e. nebulized solution and dry powder inhalation. However, the outcome of two phase II pilot studies in patients failed to demonstrate sufficient efficacy of ASM-024 in asthma and COPD. Thus, further work on ASM-024 on pulmonary diseases was stopped. In light of the findings that ASM‐024 blocks both nicotinic and muscarinic receptor activation, it is believed that ASM-024 will be a potent inhibitor of cell growth. These properties may have the potential to reduce the development or progression of tumors expressing these receptors. Based on a greater knowledge of the unique pharmacological mechanisms of action of ASM-024 developed at Asmacure, Odan is exploring the potential therapeutic role of ASM-024 in the treatment of selected oncology diseases. These studies include the in vitro anti-proliferative properties against a panel of various cancer cell lines and the in vivo anti-tumor activity in selected mouse models. Overall, the most significant inhibitory effect on in vitro cell proliferation was observed on the following cell lines: human lung adenocarcinoma, breast cancer, brain neuroblastoma, prostate adenocarcinoma and malignant melanoma. Preliminary data from a mouse model of lung carcinoma (Lewis Lung Cancer) using a slow infusion delivery method that ASM-024 treatment reduces the size and number of tumor nodules in the lung. In addition the potential therapeutic synergism between ASM-024 with commonly used chemotherapeutic agents will be investigated. Cisplatin and the taxanes (e.g. paclitaxel or Taxol) are commonly used chemotherapeutic agents, but their use is limited by their toxicity rates and innate or acquired resistance to these drugs. The concomitant effect of ASM-024 and cisplatin or Taxol on the proliferation of tumor cells will be assessed in vitro and potentially in in vivo mouse models. In the long term, Odan will consider to pursue the development of ASM-024 in a solution formulation administered intravenously (IV) in conjunction with the commonly-used cancer chemotherapeutic agents, for the growth inhibition and possibly regression of tumors in cancer patients.

Vaccenic acid (VA) (t11 octadecenoic acid) is a positional and geometric isomer of oleic acid (c9-octadecenoic acid), and is the predominant trans monoene in ruminant fats (50%–80% of total trans content). Dietary VA can be desaturated to cis-9,trans-11 conjugated linoleic acid (c9,t11-CLA) in ruminants, rodents, and humans. Hydrogenated plant oils are another source of VA in the diet, and it has been recently estimated that this source may contribute to about 13%–17% of total VA intake. In contrast to suggestions from the epidemiological studies, the majority of studies using cancer cell lines (Awad et al. 1995; Miller et al. 2003) or rodent tumors (Banni et al. 2001; Corl et al. 2003; Ip et al. 1999; Sauer et al. 2004) have demonstrated that VA reduces cell growth and (or) tumor metabolism. Animal and in vitro studies suggest that the anti-cancer properties of VA are due, in part, to the in vivo conversion of VA to c9,t11-CLA. However, several additional mechanisms for the anti-cancer effects of VA have been proposed, including changes in phosphatidylinositol hydrolysis, reduced proliferation, increased apoptosis, and inhibition of fatty acid uptake. In conclusion, although the epidemiological evidence of VA intake and cancer risk suggests a positive relationship, this is not supported by the few animal studies that have been performed. The majority of the studies suggest that any health benefit of VA may be conferred by in vivo mammalian conversion of VA to c9,t11-CLA. VA acts as a partial agonist to both peroxisome proliferator-activated receptors (PPAR)-α and PPAR-γ in vitro, with similar affinity compared to commonly known PPAR agonists. Hypolipidemic and antihypertrophic bioactivity of VA is potentially mediated via PPAR-/-dependent pathways.

PF-2545920 is an orally-active phosphodiesterase 10A (PDE10A) inhibitor originated by Pfizer, for the treatment of Huntington's disease. PF-2545920 was originally developed by Pfizer for the treatment of schizophrenia. But later clinical studies for Schizophrenia were discontinued. PF-2545920 is a potent and selective PDE10A inhibitor with IC50 of 0.37 nM, with >1000-fold selectivity over the PDE. PF-2545920 is active in a range of antipsychotic models, antagonizing apomorphine-induced climbing in mice, inhibiting conditioned avoidance responding in both rats and mice, and blocking N-methyl-D-aspartate antagonist-induced deficits in prepulse inhibition of acoustic startle response in rats, while improving baseline sensory gating in mice.