We believe that our potential therapies will have the ability to transform the lives of people with a 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 | ||
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| FHD-286 (BRG1 / BRM) |
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| FHD-286 (BRG1 / BRM) |
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| Selective BRM |
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| FHD-609 (BRD9) |
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| Selective BRM |
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| Selective ARID1B |
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| Selective CBP |
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| Undisclosed |
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| Undisclosed |
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| Partnered Program (Undisclosed) |
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| Three Discovery Programs (Undisclosed) |
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| 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 |
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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.
AML and MDS
Uveal Melanoma
BRG1 Mutated Cancers
Synovial Sarcoma & SMARCB1-Loss Tumors
BRG1 Mutated Cancers
ARID1A Mutated Cancers
EP300 Mutated Cancers
Undisclosed
Undisclosed
Undisclosed
Undisclosed
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.
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.
BRG1/BRM ATPase
Highly potent, selective, allosteric, small molecule, oral enzymatic inhibitor
Acute myeloid leukemia (AML)
Myelodysplastic syndromes (MDS)
Metastatic uveal melanoma (mUM)
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, 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.
BRD9
Highly potent, selective and intravenous, small molecule protein degrader
Synovial sarcoma
SS18-SSX1 / SSX2 / SSX4 protein fusions
We have used our Gene Traffic Control® platform to discover other programs currently in the early preclinical stage, including:
Our platform has produced a robust pipeline of diverse programs across multiple diseases.
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.