Dilmapimod is a potent p38 mitogen-activated protein kinase (MAPK) inhibitor. It was investigated for its anti-inflammatory effect in non-head injury trauma patients at risk for developing acute respiratory distress syndrome. IL-1β was identified as a gene regulated by dilmapimod that could influence c-reactive protein levels. Dilmapimod had been in phase III clinical trials by GlaxoSmithKline for the treatment of rheumatoid arthritis, neuropathic pain, coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD). However, these studies were discontinued.

Tesevatinib (EXEL-7647 or XL647) was optimized as an inhibitor of a spectrum of growth-promoting and angiogenic receptor tyrosine kinases (RTKs) to simultaneously block tumor growth and vascularization. In particular, Tesevatinib potently inhibits the EGF/ErbB2, VEGF, and ephrin RTK families. The drug is being developed by Kadmon Corporation under licence from Symphony Evolution (Symphony Capital Partners). Kadmon is developing tesevatinib for the treatment of autosomal polycystic kidney disease and solid cancers.

Crenolanib is an orally active, highly selective, small molecule, next generation inhibitor of platelet-derived growth factor receptor (PDGFR) tyrosine kinase. Crenolanib, manufactured by Arog Pharmaceuticals in Dallas, is taken orally with chemotherapy. The compound is currently being evaluated for safety and efficacy in clinical trials for various types of cancer, including acute myeloid leukemia (AML), gastrointestinal stromal tumor (GIST), and glioma. Crenolanib is an orally bioavailable, selective small molecule inhibitor of type III tyrosine kinases with nanomolar potencies against platelet-derived growth factor receptors (PDGFR) (isoforms PDGFRα and PDGFRβ) and Fms-related tyrosine kinase 3 (FLT3). Besides PDGFR and FLT3, crenolanib does not inhibit any other known receptor tyrosine kinase (RTK) (e.g. VEGFR and FGFR) or any other serine/threonine kinase (e.g., Abl, Raf) at clinically achievable concentrations. Preclinical trials have shown Crenolanib to be active in inhibiting both wild-type and mutant FLT3. Crenolanib is cytotoxic to the FLT3/ITD-expressing leukemia cell lines Molm14 and MV411, with IC50s of 7 nM and 8 nM, respectively. In immunoblots, crenolanib inhibited phosphorylation of both the wild-type FLT3 receptor (in SEMK2 cells) and the FLT3/ITD receptor (in Molm14 cells) in culture medium with IC50s of 1-3 nM. Importantly, the IC50 of crenolanib against the D835Y mutated form of FLT3 was 8.8 nM in culture medium. Furthermore, crenolanib had cytotoxic activity against primary samples that were obtained from patients who had developed D835 mutations while receiving FLT3 TKIs. In vitro, the IC50 of crenolanib for inhibition of FLT3/ITD in plasma was found to be 34 nM, indicating a relatively low degree of plasma protein binding. From pharmacokinetic studies of crenolanib in solid tumor patients, steady state trough plasma levels of roughly 500 nM were found to be safe and tolerable, suggesting that crenolanib could potentially inhibit the target in vivo. Crenolanib has no significant activity against c-KIT, which may be an advantage in that myelosuppression can be avoided.1Furthermore, there was no evidence of QTc prolongation in patients treated with crenolanib. In summary, crenolanib offers a number of advantages over other FLT3 TKIs. Clinical trials of crenolanib in AML patients with FLT3 activating mutations are being planned.

Ralimetinib (LY2228820), a trisubstituted imidazole derivative, is a potent and selective, ATP-competitive inhibitor of the α- and β-isoforms of p38 mitogen-activated protein kinase. LY2228820 produced significant tumor growth delay in multiple in vivo cancer models (melanoma, non-small cell lung cancer, ovarian, glioma, myeloma, breast). Eli Lilly is developing ralimetinib for the treatment of cancer.

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.

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.

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.

Cediranib (AZD-2171) is a VEGFR-2 kinase inhibitor which was developed by AstraZeneca for the treatment of cancer. The drug reached the final stage of approval by European Medicines Agency in 2008 under the name Zemfirza (it was recommended to be taken in combination with platinum-based chemotherapy), however on 19 September 2016 AstraZeneca decided to withdraw the Marketing Authorisation Application.

Gold monoiodide (AuI; Aurum iodatum) is a chemical compound of gold and iodine. This compound can be synthesized by heating gold and iodine in a sealed tube at 120°C for about four months. It decomposes when treated with hot water, but its related complexes are much more stable. It’s used like unapproved homeopathic product for treatment of Senile Paresis. This product is to be used for self-limiting conditions. If symptoms do not improve in 4 days, or worsen, discontinue use and seek assistance of health professional