Dana-farber-cancer Institute Inc.

The General Hospital Corporation

Yale University

Beth Israel Deaconess Medical Center, Inc.

University of Texas System

The University of North Carolina at Chapel Hill

The General Hospital Corporation D/b/a Massachusetts General Hospital

Pasi Antero Janne

Nathanael Schiander Gray

Jaebong Jang

Daniel Arie Haber

Matthew Meyerson

Thomas J Lynch

William R Sellers

Raffaella Sordella

Jeffrey E Settleman

Michael Eck

Daphne Winifred Bell

Hwan Geun Choi

Juan Guillermo Paez

John M Hatcher

Bruce E Johnson

Dries De Clercq

Tinghu Zhang

Kwok-kin Wong

Bruce E Johnston

Craig M Crews

Lewis C Cantley

David A Scott

Nathanael S Gray

Alyssa Verano

Hwangeun Choi

Sang Min Lim

Jeffrey Engelman

Jamie A Saxon

Ting Xie

Wenjun Zhou

Cloud P Paweletz

Norman E Sharpless

Nabeel Bardeesy

Ciric To

David Heppner

Diego H Castrillon

Eunyoung Park

Hongbin Ji

Jieun Son

Chelsea E Powell

Geoffrey Oxnard

Yanan Kuang

Kwok-Kin Wong

Michael J Eck

Hwanguen Choi

The application relates to a compound having Formula (I): which modulates the activity of EGFR, a pharmaceutical composition comprising the compound, and a method of treating or preventing a disease in which EGFR plays a role.

Pyrimidines as EGFR-inhibitors and methods of treating disorders

Disclosed are bispecific compounds (degraders) that target ALK for degradation. Also disclosed are pharmaceutical compositions containing the degraders and methods of using the compounds to treat diseases and disorders characterized or mediated by aberrant ALK activity.

Degraders that target ALK and therapeutic uses thereof

Disclosed herein are methods and reagents for determining the responsiveness of cancer to an epidermal growth factor receptor (EGFR) targeting treatment. The detection of these mutations will allow for the administration of gefitinib, erlotinib and other tyrosine kinase inhibitors to those patients most likely to respond to the drug.

Method to determine responsiveness of cancer to epidermal growth factor receptor targeting treatments

The application relates to a compound having Formula X: which modulates the activity of HER2 and/or a mutant thereof, and/or EGFR and/or a mutant thereof, a pharmaceutical composition comprising the compound, and a method of treating or preventing a disease in which HER2 and/or a mutant thereof, and/or EGFR and/or a mutant thereof, plays a role.

Inhibitors of EGFR and/or HER2 and methods of use

The application relates to a compound of Formula (I): which modulates the activity of ALK or SRPK, a pharmaceutical composition comprising the compound, and a method of treating or preventing a disease in which ALK or SRPK plays a role.

Substituted 6,11-dihydro-5H-benzo[b]carbazoles as inhibitors of ALK and SRPK

The application relates to a compound having Formula I: which modulates the activity of HER2 and/or a mutant thereof, a pharmaceutical composition comprising the compound, and a method of treating or preventing a disease in which HER2 and/or a mutant thereof plays a role.

Cyano quinoline amide compounds as HER2 inhibitors and methods of use

Pyrimidines as EGFR inhibitors and methods of treating disorders

The application relates to a compound having Formula Ia or Ib: or a pharmaceutically acceptable salt, hydrate, or solvate thereof, which modulates the activity of EGFR, a pharmaceutical composition comprising the compound, and a method of treating or preventing a disease in which EGFR plays a role. 

Inhibitors of EGFR and methods of use thereof

The application relates to a compound having Formula X: which modulates the activity of HER2 and/or a mutant thereof, and/or EGFR and/or a mutant thereof, a pharmaceutical composition comprising the compound, and a method of treating or preventing a disease in which HER2 and/or a mutant thereof, and/or EGFR and/or a mutant thereof, plays a role. 

The present application provides bifunctional compounds of Formula (I): which act as protein degradation inducing moieties for EGFR and/or a mutant thereof. The present application also describes methods for the targeted degradation of EGFR and/or a mutant thereof through the use of the bifunctional compounds that link a ubiquitin ligase-binding moiety to a ligand that is capable of binding to EGFR and/or a mutant thereof which can be utilized in the treatment of disorders modulated by EGFR or a mutant thereof.

Bifunctional molecules for degradation of EGFR and methods of use

Substituted 6,11-dihydro-5H-benzo[B]carbazoles as inhibitors of ALK and SRPK

Provided herein are methods for treating cancer that is resistant to treatment with an anti-ErbB therapeutic agent and which is associated with an activating MET gene mutation or a MET gene amplification. The methods involve administering to a subject a combination of an anti-ErbB therapeutic and an anti-MET therapeutic. Also provided are methods for reducing ErbB mediated signaling or PI3 kinase mediated signaling in a cancer cell.

Methods for treating cancer resistant to ErbB therapeutics

The present invention provides methods of detecting cancer using biomarkers.

Methods of diagnosing and prognosing lung cancer

The invention provides methods to monitor cell free nucleic acids. The method comprises obtaining a plasma sample from a subject known to have a cancer characterized by a pair of mutually exclusive mutations specific to the cancer; isolating cell free nucleic acids from the plasma sample obtained from the subject; measuring the amount a housekeeping gene and/or total DNA in the cell free nucleic acids isolated from the plasma sample to confirm that the amount of housekeeping gene and/or total DNA in the sample is within a selected range; measuring the amount of a first of the pair of mutually exclusive mutations specific to the cancer in the cell free nucleic acids isolated from the plasma sample; and indicating in a report that the subject has the first mutation when (a) the amount of the housekeeping gene and/or total DNA in the cell free nucleic acids isolated from the plasma sample is within the selected range and (b) the amount of the first mutation is increased as compared to a control amount, wherein the control amount is determined by measuring the apparent amount of the first mutation in control cell free nucleic acids isolated from plasma samples obtained from control subjects known to have the second of the pair of mutually exclusive mutations specific to the cancer using measuring conditions substantially the same as those used to measure the amount of the first mutation in the cell free nucleic acids isolated from the plasma sample from the subject.

Non-invasive blood based monitoring of genomic alterations in cancer

Growing community of inventors

Newton, MA, United States of America

Pasi Antero Janne