Toceranib (toceranib phosphate) is an orally bioavailable small molecule inhibitor that blocks a variety of RTKs, including VEGFR2, PDGFRa and KIT. In non-clinical pharmacology studies, toceranib selectively inhibited the tyrosine kinase activity of several members of the split kinase receptor tyrosine kinase (RTK) family, some of which are implicated in tumor growth, pathologic angiogenesis, and metastatic progression of cancer. Toceranib inhibited the activity of Flk-1/KDR tyrosine kinase (vascular endothelial growth factor receptor, VEGFR2), platelet-derived growth factor receptor (PDGFR), and stem cell factor receptor (Kit) in both biochemical and cellular assays. Toceranib has been shown to exert an antiproliferative effect on endothelial cells in vitro. Toceranib treatment can induce cell cycle arrest and subsequent apoptosis in tumor cell lines expressing activating mutations in the split kinase RTK, ckit. Canine mast cell tumor growth is frequently driven by activating mutations in c-kit. Toceranib is a dog-specific anti-cancer drug approved by the U.S. Food and Drug Administration. It is marketed as Palladia as its phosphate salt, toceranib phosphate by Pfizer. PALLADIA (Toceranib) tablets are indicated for the treatment of Patnaik grade II or III, recurrent, cutaneous mast cell tumors with or without regional lymph node involvement in dogs.

Adenine is a nucleobase (a purine derivative). Its derivatives have a variety of roles in biochemistry including cellular respiration, in the form of both the energy-rich adenosine triphosphate (ATP) and the cofactors nicotinamide adenine dinucleotide (NAD) and flavin adenine dinucleotide (FAD). It also has functions in protein synthesis and as a chemical component of DNA and RNA. The shape of adenine is complementary to either thymine in DNA or uracil in RNA

Ethoxyquin (EQ) has been used as an antioxidant in animal feed for many years, but pharmacological use of EQ has never been evaluated in humans despite that small amounts of EQ exist in certain food items. The level of this antioxidant in animal feeds should not be higher than 150 ppm (U.S. FDA permissions). Ethoxyquin is rapidly absorbed from gastrointestinal tract of laboratory animals like rats and mice. Peak blood concentration of the compound is observed within 1 h. Distribution of EQ in animal body is similar when it is administered orally and intravenously. Small amounts of parent EQ were detected in liver, kidney, and adipose tissue and fish muscles. It is excreted predominantly as metabolites via urine. Ethoxyquin is also registered as an antioxidant to control scald (browning) in apples and pears. EQ-induced DNA damage in human lymphocytes in a dose-dependent manner. According to the studies on dogs and laboratory animals it was shown that ethoxyquin had little acute toxicity, except when it is administered parenterally. Values of LD50 for EQ are 1700 mg kg−1 bw (rats, oral gavage), 2000 mg kg−1 bw (rats, dermal treatment, 24 h), 900 mg kg−1 bw (mice, intraperitoneal administration), and 180 mg kg−1 bw (mice, intravenous administration).

TILIDINE is a low to medium potency opioid analgesic. It is metabolized to its active metabolites, nortilidine and bisnortilidine. Its analgesic activity is largely exerted through nortilidine which is a potent agonist at Mu opioid receptors.

Bucladesine is a cyclic nucleotide derivative which mimics the action of endogenous cAMP and is a phosphodiesterase inhibitor. The compound is used in a wide variety of research applications because it mimics cAMP and can induce normal physiological responses when added to cells in experimental conditions. cAMP is only able to elicit minimal responses in these situations. The neurite outgrowth instigated by bucladesine in cell cultures has been shown to be enhanced by nardosinone. Recently, the effect of bucladesine as a cAMP analog has been studied on the pentylenetetrazol-induced seizure in the wild-type mice. The data showed that bucladesine (300nM/mouse) reduced the seizure latency and threshold. In addition they found that combination of bucladesine and pentoxyfillin has additive effect on seizure latency and threshold. Bucladesine is more lipophilic than cAMP and in contrast to cAMP capable of penetrating cell membranes. Bucladesine interferes with different protein kinases which are normally activated by cAMP. Bucladesine has undergone in the past clinical developments as systemic treatment for cardioprotection and as topical treatment to improve wound healing. In Japan, a bucladesine ointment (Actosin® ointment; Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan) was marketed to treat skin ulcers. Clinical studies have shown favourable effects on diabetic foot ulcers or decubitus, but the compound was later withdrawn despite good tolerability. One possible reason for the withdrawal may be the odour of the cream formulation which can be related to the hydrolytic cleavage in aqueous solutions resulting in release of butyric acid.

Piperaquine is a bisquinoline antimalarial drug that was first synthesized in the 1960s and used extensively in China and Indochina as prophylaxis and treatment during the next 20 years. Usage declined in the 1980s as piperaquine-resistant strains of P. falciparum arose and artemisinin-based antimalarials became available. However, during the next decade, piperaquine was rediscovered by Chinese scientists as one of a number of compounds suitable for combination with an artemisinin derivative. The rationale for such artemisinin combination therapies (ACTs) was to provide an inexpensive, short-course treatment regimen with a high cure rate and good tolerability that would reduce transmission and protect against the development of parasite resistance. Piperaquine is characterized by slow absorption and a long biological half-life, making it a good partner drug with artemisinin derivatives which are fast acting but have a short biological half-life.

Aminopropyl racementhyl phosphate is a prodrug of menthol patented by Pacific Corporation (Korea). Upon administration, it is enzymatically decomposed into menthol and 3-aminopropylphosphoric acid, a component used for anti-aging cosmetic composition. Aminopropyl racementhyl phosphate was found to reduce the irritation of menthol while maintaining its useful effects.

Sodium glycerol 2-phosphate (Disodium beta-glycerophosphate) is used for the preparation of thermo-sensitive chitosan hydrogen as a scaffold to construct tissue engineered injectable nucleus pulposus (NP). Since Sodium glycerol 2-phosphate (6 g/day) reduced the lithogenic index of bile in human subjects with cholesterol gallstones in a short-term study and facilitated dissolution of cholesterol gallstones in mice, Sodium glycerol 2-phosphate may have potential to help dissolve cholesterol gallstones in man. Sodium glycerol 2-phosphate is an alkaline phosphate inhibitor. Sodium β-glycerophosphate pentahydrate is used as a phosphatase inhibitor. It promotes bone matrix mineralization while delivering to osteoblasts by providing a source of phosphate ions. It is used in the development of hydrogels and scaffolds, which finds applications in tissue engineering and cell growth. It is used as an additive in isolation mediums by providing phosphate ions to isolate. It is utilized to promote mineralization in vitro by modulating bone cell metabolic activity.

Isaxonine (N-isopropyl-amino-2-pyrimidine orthophosphate) is able to accelerate nerve regeneration and functional recovery. Isaxonine has specific affinity for peripheral nerves. It acts directly on the neuron or indirectly by stimulating the production of a growth factor remains unknown. It demonstrates activity in the treatment of neuropathies of various etiology. Isaxonine treatment may be associated with hepatotoxicity.

Creatinolfosfate (or creatinol-O-phosphate, or COP) possesses anti-ischemic and anti-arrhythmic activities associated with improved ionic balance and heart performance. This compound exerts its cardioprotective effect by action on anaerobic glycolysis. The results of the toxicological studies showed that creatinolfosfate didn’t have side effects.