OUR PIPELINE

We believe that our potential therapies will have the ability to transform the lives of people with a wide spectrum of diseases, including many types of cancer. Through our pipeline of proprietary enzymatic inhibitors, targeted protein degraders, and transcription factor disruptors, we are building the next wave of precision therapies.

Program/Target Indication Discovery IND-enabling Phase 1 Phase 2 Phase 3 Global Rights
FHD-286
(BRG1 / BRM)
AML Combination Study
Foghorn Therapeutics
Selective BRM
BRG1 Mutated Cancers
Foghorn Therapeutics and Loxo Oncology at Lilly
FHD-286
(BRG1 / BRM)

- Not advancing independently
Uveal Melanoma
Foghorn Therapeutics
Selective BRM
BRG1 Mutated Cancers
Foghorn Therapeutics and Loxo Oncology at Lilly
Selective ARID1B
ARID1A Mutated Cancers
Foghorn Therapeutics
Selective CBP
EP300 Mutated Cancers
Foghorn Therapeutics
Selective EP300
CBP Mutated & Subsets of EP300 Dependent Cancers
Foghorn Therapeutics
FHD-609 (BRD9)

- Partial Clinical Hold
Synovial Sarcoma & SMARCB1-Loss Tumors
Foghorn Therapeutics
Undisclosed
Undisclosed
Foghorn Therapeutics
Undisclosed
Undisclosed
Merck
Partnered Program (Undisclosed)
Undisclosed
Foghorn Therapeutics and Loxo Oncology at Lilly
3 Discovery Programs (Undisclosed)
Undisclosed
Foghorn Therapeutics and Loxo Oncology at Lilly
Additional Discovery  

Using our proprietary Gene Traffic Control® platform, we have identified additional genetically determined dependencies to drug using enzymatic inhibitors, protein degraders and transcription factor disruptors

 

While initially focused on the BAF chromatin regulatory complex, we believe our platform is broadly applicable to other chromatin remodeling complexes, other transcription factors, and other diseases.

  • Enzyme Inhibitors
  • Protein Degraders
  • Transcription Factor Disruptors
  • Undisclosed
  • Enzyme Inhibitors
  • Protein Degraders
  • Transcription Factor Disruptors
  • Undisclosed
FHD-286
(BRG1 / BRM)
Global Rights: Foghorn Therapeutics

AML Combination Study

Phase 1
Selective BRM
Global Rights: Foghorn Therapeutics

BRG1 Mutated Cancers

IND-enabling
FHD-286
(BRG1 / BRM)

- Not advancing independently
Global Rights: Foghorn Therapeutics

Uveal Melanoma

Phase 1
Selective BRM
Global Rights: Foghorn Therapeutics

BRG1 Mutated Cancers

IND-enabling
Selective ARID1B
Global Rights: Foghorn Therapeutics

ARID1A Mutated Cancers

IND-enabling
Selective CBP
Global Rights: Foghorn Therapeutics

EP300 Mutated Cancers

IND-enabling
Selective EP300
Global Rights: Foghorn Therapeutics

CBP Mutated & Subsets of EP300 Dependent Cancers

IND-enabling
FHD-609 (BRD9)

- Partial Clinical Hold
Global Rights: Foghorn Therapeutics

Synovial Sarcoma & SMARCB1-Loss Tumors

Phase 1
Undisclosed
Global Rights: Foghorn Therapeutics

Undisclosed

IND-enabling
Undisclosed
Global Rights: Foghorn Therapeutics

Undisclosed

IND-enabling
Partnered Program (Undisclosed)
Global Rights: Foghorn Therapeutics

Undisclosed

IND-enabling
3 Discovery Programs (Undisclosed)
Global Rights: Foghorn Therapeutics

Undisclosed

IND-enabling
Additional Discovery

Using our proprietary Gene Traffic Control® platform, we have identified additional genetically determined dependencies to drug using enzymatic inhibitors, protein degraders and transcription factor disruptors

While initially focused on the BAF chromatin regulatory complex, we believe our platform is broadly applicable to other chromatin remodeling complexes, other transcription factors, and other diseases.

OUR LEAD CANDIDATES

FHD-286

FHD-286, is an enzymatic inhibitor of BRG1 and BRM, which are two highly similar proteins that are the ATPases, or catalytic engines, across all forms of the BAF complex. Every BAF complex includes either BRG1 or BRM. FHD-286 inhibits the function of BRG1 and BRM in cancers that are heavily dependent on BRG1 and BRM.

Target & Modality

BRG1/BRM ATPase

Highly potent, selective, allosteric, small molecule, oral enzymatic inhibitor

Initial Indications

Acute myeloid leukemia (AML)

Myelodysplastic syndromes (MDS)

Metastatic uveal melanoma (mUM)

Genetic Dependency

AML: Elevated BRG1-BAF / TF activity in AML blast cells

Uveal melanoma: GNAQ / GNA11 mutated UM is driven by dependency on BAF / TF activity

FHD-609

FHD-609, is a protein degrader of BRD9. BRD9 is a component of one form of the BAF complex. Nearly all synovial sarcoma cancers contain a translocation, a type of mutation, between a BAF subunit gene, SS18, and another set of genes. This mutation causes cancer cells to rely on BRD9 for their survival.

FHD-609 has two domains: one that binds to BRD9 and the other that binds to a complex that directs proteins for destruction. By targeting BRD9 for degradation, FHD-609 depletes a key subunit of the BAF complex that is required for the survival of cancer cells.

Target & Modality

BRD9

Highly potent, selective and intravenous, small molecule protein degrader

Initial Indications

Synovial sarcoma

Genetic Dependency

SS18-SSX1 / SSX2 / SSX4 protein fusions

Preclinical & Discovery Programs

We have used our Gene Traffic Control® platform to discover other programs currently in the early preclinical stage, including:

  • A selective BRM inhibitor and degrader, which targets cancers with mutations in the BRG1 subunit of the BAF complex.
  • An ARID1B degrader, which targets cancers with mutations in ARID1A subunit of the BAF complex.
  • Compounds that disrupt the interactions between transcription factors and chromatin remodeling complexes.

Our Pipeline

Our platform has produced a robust pipeline of diverse programs across multiple diseases.

OUR COLLABORATIONS

Our collaboration with Loxo Oncology at Lilly includes a co-development and co-commercialization agreement on the selective BRM oncology program and an additional undisclosed oncology target. In addition, the partnership includes three additional discovery programs using Foghorn’s proprietary Gene Traffic Control® platform.

Our approach to disrupting the interactions between transcription factors and the chromatin remodeling complex is the basis of a collaboration with Merck. In this collaboration, we will use our platform to identify disruptors of one specific transcription factor.

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