Wang Ling

Bio: Wang Ling is an academic researcher. The author has contributed to research in topics: Receptor tyrosine kinase & Trk receptor. The author has an hindex of 1, co-authored 2 publications receiving 64 citations.

Compositions of protein receptor tyrosine kinase inhibitors

Abstract: The present invention relates to novel synthetic substituted heterocyclic compounds and pharmaceutical compositions containing the same that are capable of inhibiting or antagonizing a family of receptor tyrosine kinases, Tropomysosin Related Kinases (Trk), in particular the nerve growth factor (NGF) receptor, TrkA. The invention further concerns the use of such compounds in the treatment and/or prevention of pain, cancer, restenosis, atherosclerosis, psoriasis, thrombosis, or a disease, disorder or injury relating to dysmyelination or demyelination or the disease or disorder associated with abnormal activities of NGF recptor TrkA.

Protein receptor tyrosine kinase inhibitor composition

Abstract: PROBLEM TO BE SOLVED: To provide a protein receptor tyrosine kinase inhibitor.SOLUTION: The present invention relates to a novel synthesis substituted heterocyclic compound and pharmaceutical composition containing the same that can inhibit or antagonize a receptor tyrosine kinase family, Tropomyosin (Tropomysosin) related kinase (Trk), particularly nerve growth factor (NGF) receptor, TrkA. And further, the present invention also relates to a use of said compound in the treatment and/or prophylaxis of pain, cancer, restenosis, atherosclerosis, psoriasis, thrombosis, or a disease, disorder or damage associated with dysmyelination or demyelination, or a disease or disorder associated with NGF receptor TrkA abnormal activity.SELECTED DRAWING: None

Heterocyclic compounds and uses thereof

Abstract: Compounds and pharmaceutical compositions that modulate kinase activity, including PI3 kinase activity, and compounds, pharmaceutical compositions, and methods of treatment of diseases and conditions associated with kinase activity, including PI3 kinase activity, are described herein.

Substituted isoquinolinones and quinazolinones

Abstract: The invention relates to substituted nitrogen containing bicyclic heterocycles of the formula (I): wherein Z is CH2 or N-R4 and X, R1, R2, R4, R6, R7 and n are as defined in the description. Such compounds are suitable for the treatment of a disorder or disease which is mediated by the activity of MDM2 and/or MDM4, or variants thereof.

Fused heterocyclic compounds as ion channel modulators

Abstract: The present disclosure relates to compounds that are sodium channel inhibitors and to their use in the treatment of various disease states, including cardiovascular diseases and diabetes. In particular embodiments, the structure of the compounds is given by Formula I: wherein X, Y, Z, R2, R3, R4, p and q are as described herein, to methods for the preparation and use of the compounds and to pharmaceutical compositions containing the same.

Pyrrolidinyl urea, thiourea, guanidine and cyanoguanidine compounds as TrkA kinase inhibitors

Abstract: Compounds of Formula I: or stereoisomers, tautomers, or pharmaceutically acceptable salts, solvates or prodrugs thereof, wherein Ring A, Ring C and X are as defined herein, are inhibitors of TrkA kinase and are useful in the treatment of diseases which can be treated with a TrkA kinase inhibitor such as pain, cancer, inflammation/inflammatory diseases, neurodegenerative diseases, certain infectious diseases, Sjogren's syndrome, endometriosis, diabetic peripheral neuropathy, prostatitis or pelvic pain syndrome.

TrkA kinase inhibitors, compositions and methods thereof

Abstract: The present invention is directed to benzyl urea compounds of formula (I) which are tropomyosin-related kinase (Trk) family protein kinase inhibitors, and hence may be useful in the treatment of pain, inflammation, cancer, restenosis, atherosclerosis, psoriasis, thrombosis, a disease, disorder, injury, or malfunction relating to dysmyelination or demyelination or a disease or disorder associated with abnormal activities of nerve growth factor (NGF) receptor Trk-A, Trk-B and/or Trk-C.