AZD2932 is an oral inhibitor of VEGFR-2 and PDGFR tyrosine kinases, which was developed by AstraZeneca as a potential anti-cancer medicine. The drug was tested in vivo in preclinical model of mice bearing C6 rat glial tumors and AZD2932 demonstrated good potency: growth of Calu-6 tumor was inhibited by 81% and 72% at 50 and 12.5 mg/kg b.i.d. and LoVo tumors by 67% at 50 mg/kg b.i.d.

CP-673,451 is a potent inhibitor of platelet-derived growth factor beta-receptor (PDGFR-beta) kinase- and PDGF-BB-stimulated autophosphorylation of PDGFR-beta in cells. CP 673451 in a sponge implant model where a surgical sponge was soaked with PDGFBB to initiate angiogenesis, CP 673451 inhibited 75% of PDGF-BB-stimulated angiogenesis at a dose of 3 mg/kg for 5 days. CP 673451 did not inhibit angiogenesis induced by either VEGF or bFGF in the sponge. CP 673451 also inhibited tumour growth in H460 human lung carcinoma, Colo205 and LS174T human colon carcinomas and U87MG human glioblastoma multiforme xenograft models. CP-673,451 has not been studied in clinical trials due to issues with toxicity in preclinical studies.

N-Desethyl Sunitinib is a major and pharmacologically active metabolite of sunitinib, which is potent, ATP-competitive VEGFR, PDGFRβ, and KIT inhibitor.

Polaprezinc is a zinc-containing molecule and used for the therapy of gastric ulcer. It has been reported that this compound inhibits the induction of TNF-a as well as cellular signaling of TNF-a. Polaprezinc has been shown to exert an anti-oxidant property in a tube experiment and accelerate the healing of gastric ulcer in humans. Polaprezinc inhibited EtOH-induced cytochrome c reduction. Protection by polaprezinc was microscopically associated with the prevention of monolayer disruption. In an animal model of chemotherapy-induced oral mucositis polaprezinc improves the recovery from 5-fluorouracil–induced oral mucositis in hamsters. Polaprezinc ameliorates mucosal ulceration in acetic acid-induced experimental oral mucositis in hamsters. Polaprezinc is potentially useful for prevention of oral mucositis and improvement of quality of life without reducing the tumor response. Polaprezinc is in phase II clinical trial for the treatment of taste disorders.

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.

Masitinib is a new orally administered tyrosine kinase inhibitor that targets mast cells and macrophages, important cells for immunity, through inhibiting a limited number of kinases. Based on its unique mechanism of action, masitinib can be developed in a large number of conditions in oncology, in inflammatory diseases, and in certain diseases of the central nervous system. In oncology due to its immunotherapy effect, masitinib can have an effect on survival, alone or in combination with chemotherapy. Through its activity on mast cells and consequently the inhibition of the activation of the inflammatory process, masitinib can have an effect on the symptoms associated with some inflammatory and central nervous system diseases and the degeneration of these diseases. AB Science is developing masitinib in multiple sclerosis and alzheimer's disease. Masitinib targets kinases, including c-Kit, PDGFR, and Lyn. It is used in the treatment of mast cell tumors in animals, specifically dogs. Since its introduction in November 2008 it has been distributed under the commercial name Masivet. It has been available in Europe since the second part of 2009. In the USA it is distributed under the name Kinavet.

AL3818 (anlotinib) is a receptor tyrosine kinase inhibitor targeting vascular endothelial growth factor receptors (VEGFR1, VEGFR2/KDR, and VEGFR3), stem cell factor receptor (C-kit), platelet-derived growth factor (PDGFβ), and fibroblast growth factor receptors (FGFR1, FGFR2, and FGFR3). Anlotibib is a kind of innovative medicines approved by State Food and Drug Administration（SFDA:2011L00661) which was researched by Jiangsu Chia-tai Tianqing Pharmaceutical Co., Ltd. Phase III development is underway for the treatment of thyroid cancer, gastric cancer, leiomyosarcoma; non-small cell lung cancer; synovial sarcoma; thyroid cancer etc.

Trapidil, a platelet-derived growth factor antagonist, was originally developed as a vasodilator and anti-platelet agent and has been used to treat patients with ischemic coronary heart, liver, and kidney disease. Used to treat patients with ischemic coronary heart, liver, and kidney disease.

Quizartinib (AC220) is an orally bioavailable, small molecule receptor tyrosine kinase inhibitor that is being developed by Daiichi Sankyo Company (previously Ambit Biosciences) and Astellas Pharma as a treatment for acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL) and advanced solid tumours. The highest affinity target identified for Quizartinib was FLT3. The only other kinases with binding constants within 10-fold that for FLT3 were the closely related receptor tyrosine kinases KIT, PDGFRA, PDGFRB, RET, and CSF1R. Kinase inhibition of (mutant) KIT, PDGFR and FLT3 isoforms by quizartinib leads to potent inhibition of cellular proliferation and induction of apoptosis in in vitro leukemia models as well as in native leukemia blasts treated ex vivo.