H. Lee Moffitt Cancer Center and Research Institute, Inc.

University of South Florida

University of Central Florida Research Foundation Inc

Nicholas James Lawrence

Harshani Lawrence

Said M Sebti

James Turkson

Ernst Schönbrunn

Srikumar Chellappan

Wayne Charles Guida

Nupam Mahajan

Man Lun Yip

Sujeewa Ranatunga Mahanthe Mudiyanselage

Benjamin Greedy

Pearlie Burnette

Gary Reuther

Kiran N Mahajan

Jie Wu

Claudio Anasetti

Brian Betts

Roberta Pireddu

Matthew P Martin

Joseph Pidala

Ernst Shönbrunn

Gregory Springett

Disclosed herein are compounds that are inhibitors of BDR4 and their use in the treatment of cancer. Methods of screening for selective inhibitors of BDR4 are also disclosed. In certain aspects, disclosed are compounds of Formula I through IV.

BRD4-JAK2 inhibitors

Disclosed are small molecules against cereblon to enhance effector T cell function. Methods of making these molecules and methods of using them to treat various disease states are also disclosed.

Dimeric immuno-modulatory compounds against cereblon-based mechanisms

Disclosed herein are compounds that are inhibitors of BDR4 and their use in the treatment of cancer. Methods of screening for selective inhibitors of BDR4 are also disclosed. In certain aspects, disclosed are compounds of Formula I, II, and II.

Disclosed herein are compounds and methods for reducing the risk of developing, preventing, or treating graft versus host disease (GVHD) in a subject. The compounds can concurrently block Aurora kinase A and JAK2 signal transduction which synergistically suppresses alloreactive human T-cells in vitro, prevents xenogeneic graft-versus-host disease without impairing anti-tumor responses, and promotes the development and suppressive potency of CD39+ inducible T. In certain aspects, disclosed are compounds of Formula I-V.

Aurora kinase and janus kinase inhibitors for prevention of graft versus host disease

Binding of the transcriptional co-activator, YAP1, to the transcription factor Oct4, induces Sox2, which is a transcription actor necessary for the self-renewal of stem-like cells from non-small cell lung cancer. The WW domain of YAP1 binds to the PPxY motif of Oct4 to induce Sox2. Delivering a peptide corresponding to the WW domain could prevent the induction of Sox2 and sternness. Similarly, peptides and mimetics of the PPxY motif would be able to inhibit sternness. Disclosed are compounds that affect the Yap1:Oct4 interaction.

YAP1 inhibitors that target the interaction of YAP1 with OCT4

Disclosed is a method for selecting a cancer therapeutic for a patient that involves assaying a tumor biopsy sample from the subject to detect PAXIP1 expression, and selecting a WEE1 inhibitor as the cancer therapeutic if PAXIP1 is detected in the tumor biopsy sample.

Allosteric inhibitor of WEE1 kinase

BRD4-kinase inhibitors as cancer therapeutics

The subject invention concerns a compound and compositions having activity as an inhibitor of Stat3 protein and methods of using the compound and compositions. In one embodiment, a compound of the invention has the structure shown in formula I, formula II, or formula III. The subject invention also concerns methods of using the compounds and compositions of the invention.

Platinum compounds that inhibit constitutive STAT3 signaling and induce cell cycle arrest and apoptosis of malignant cells

Binding of the transcriptional co-activator, YAP1, to the transcription factor Oct4, induces Sox2, which is a transcription actor necessary for the self-renewal of stem-like cells from non-small cell lung cancer. The WW domain of YAP1 binds to the PPxY motif of Oct4 to induce Sox2. Delivering a peptide corresponding to the WW domain could prevent the induction of Sox2 and stemness. Similarly, peptides and mimetics of the PPxY motif would be able to inhibit sternness. Disclosed are compounds that affect the Yap1:Oct4 interaction.

YAP1 inhibitors that target the interaction of YAP1 with Oct4

Small molecules against cereblon to enhance effector t cell function

Disclosed herein are compounds and methods for reducing the risk of developing, preventing, or treating graft versus host disease (GVHD) in a subject. The compounds can concurrently block Aurora kinase A and JAK2 signal transduction which synergistically suppresses alloreactive human T-cells in vitro, prevents xenogeneic graft-versus-host disease without impairing anti-tumor responses, and promotes the development and suppressive potency of CD39+ inducible T. In certain aspects, disclosed are compounds of Formula I-V. 

Aurora kinase and Janus kinase inhibitors for prevention of graft versus host disease

The subject matter disclosed herein relates to compositions and methods of making and using the compositions. In a further aspect, the subject matter disclosed herein relates to inhibitors of STAT3 dimerization. Methods of making these compositions as well as compositions comprising these compositions are also disclosed. Also disclosed are methods of treating or preventing certain cancers by administering to an individual in need thereof and effective amount of the compounds disclosed herein. Still further, disclosed herein are methods of inhibiting STAT3 by contacting a cell with a compound or composition as disclosed herein.

STAT3 dimerization inhibitors

Binding of the transcriptional co-activator, YAP1, to the transcription factor Oct4, induces Sox2, which is a transcription actor necessary for the self-renewal of stem-like cells from non-small cell lung cancer. The WW domain of YAP1 binds to the PPxY motif of Oct4 to induce Sox2. Delivering a peptide corresponding to the WAV domain could prevent the induction of Sox2 and stemness. Similarly, peptides and mimetics of the PPxY motif would be able to inhibit stemness. Disclosed are compounds that affect the Yap1:Oct4 interaction.

Growing community of inventors

Tampa, FL, United States of America

Nicholas James Lawrence