Plexxikon Inc.

Onyx Pharmaceuticals, Inc.

Gideon Bollag

Prabha N Ibrahim

Klaus-Peter Hirth

Jiazhong Zhang

Chao Zhang

Hanna Cho

Wayne Spevak

Brian L West

Dean R Artis

Ryan Bremer

Guoxian Wu

Shumeye Mamo

Shenghua Shi

Samuel J Gillette

Paul Lin

Marika Nespi

Gaston G Habets

James Tsai

Jianming Tsai

Ying Zhang

Yong-Liang Zhu

Songyuan Shi

Jack Lin

Todd Ewing

Rebecca Zuckerman

Hongyao Zhu

Anne M Crompton

Anne North

Yoshihisa Suzuki

John F Lyons

Sanju Sharma

William Roscoe

Yoshisa Suzuki

The present disclosure provides methods of using protein kinase inhibitors for treating diseases and conditions, including diseases and conditions associated with activity of any protein kinase selected from Fms protein kinase including any mutations thereof, Kit protein kinase any mutations thereof, Flt-3 protein kinase any mutations thereof and combinations thereof.

Kinase modulation, and indications therefor

The present disclosure provides methods of treating a subject suffering from or at risk of a BRAF V600 mutation or BRAF fusion mutation related disease or condition, without activating the MAPK pathway or inducing expression of MAPK pathway genes in cells harboring wild-type BRAF.

Compounds, compositions and methods useful for treatment of Flt3-mediated diseases or conditions are provided herewith. Also provided herewith are methods for modulating the receptor protein tyrosine like kinase 3(Flt3).

Kinase modulation and indications therefor

Compounds active on protein kinases are described, as well as methods of using such compounds to treat diseases and conditions associated with aberrant activity of protein kinases.

Compounds and methods for kinase modulation, and indications therefor

Materials and methods for treating certain cancers are described, preferably cancers that result from the up-regulation of the RAF-MEK-ERK pathway, and more preferably chronic myelogenous leukemia, and which cancer is preferably resistant to the inhibition of the Bcr-Abl tyrosine kinase, imatinib.

RAF-MEK-ERK pathway inhibitors to treat cancer

Methods and compositions are described that affect the GTPase activity of members of the Ras superfamily, preferably Rac, such compositions include guanine nucleotide exchange factors that modulate the GTPase activity, preferably in the presence of GEF enhancers, exemplary guanine nucleotide exchange factors being Rac-GEF and Tiam-1, which are encoded by certain nucleic acid sequences that are herein described, along with uses for the guanine nucleotide exchange factors and the nucleic acid sequences including screening for ligands which recognize Rac-GEF, regulators of Rac-GEF activity, and methods of treating pathological conditions associated or related to a Ras superfamily GTPase, including Rac.

Methods and compositions for treating abnormal cell growth related to unwanted guanine nucleotide exchange factor activity

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Orinda, CA, United States of America

Gideon Bollag