Our Vision

Precision Cancer Medicines for
Every Genetically Defined Patient

Company Overview

Black Diamond Therapeutics: A Precision Oncology Medicine Company Pioneering the Discovery of Small Molecule, Tumor-Agnostic Therapies

Black Diamond Therapeutics is a precision oncology medicine company pioneering the discovery and development of small molecule, tumor-agnostic therapies. Black Diamond targets undrugged mutations in patients with genetically defined cancers for whom limited treatment options currently exist. Black Diamond is built upon a deep understanding of cancer genetics, protein structure and function, and medicinal chemistry. The Company’s proprietary technology platform, Mutation-Allostery-Pharmacology, or MAP, platform, is designed to allow Black Diamond to analyze population-level genetic sequencing data to identify oncogenic mutations that promote cancer across tumor types, group these mutations into families and develop a single small molecule therapy in a tumor-agnostic manner that targets a specific family of mutations.

Black Diamond was founded by David M. Epstein, Ph.D., and Elizabeth Buck, Ph.D., and starting in 2017, together with Versant Ventures, began building its MAP platform and chemistry discovery engine. Black Diamond was the first company to emerge from Versant’s Ridgeline Discovery Engine in Basel, Switzerland. Versant’s Ridgeline team of scientists, including Alex Mayweg, Ph.D., Fang Ni, Pharm.D, Alexander Flohr, Ph.D., Roberto Iacone, Ph.D., Giorgio Ottaviani, Ph.D., DABT, along with Black Diamond scientist Matthew O’Connor, were instrumental in helping us define our drug discovery strategies, identify our initial core programs, develop our lead candidate BDTX-189, and validate our MAP platform.

The cornerstone of our approach derives from evolving trends in targeted oncology therapies. Genetic sequencing of cancers has become increasingly widespread, leading to the discovery of multiple genetic alterations which were previously unaddressed, unsuccessfully targeted or overlooked. Today, new baskets of undrugged oncogenic targets have been identified, revealing a significant unmet medical need for novel targeted therapies that can extend precision medicines to patients with cancer.

Black Diamond's MAP Platform

Discover, Uncover and Target

Mutations

null

Black Diamond Therapeutics mines mutational hotspots for allosteric sites that produce potent oncogenes

Our computational platform integrates multiple forms of genome-level data with a deep understanding of mechanism, structure and dynamics.

Allostery

null

Black Diamond's platform provides insights into how allosteric mutations drive oncogenic activation

Allosterically activated oncogenes are identified by mapping mutation onto regulatory domains and regions involved protein-protein interfaces.

Protein Pharmacology

null

Black Diamond Therapeutics exploits this unique pharmacology to design drugs that are potent and selective for allosteric mutant oncogenes

Allosteric oncogenes are validated through screening in proprietary models of cancer.

The Science of Black Diamond

What is an allosteric mutation?

An allosteric mutation occurs distal to the site of action of an enzyme or receptor. In receptor tyrosine kinases, allosteric mutations occur distal to the the ATP binding site. 

Because large-scale conformational changes in proteins are a prerequisite for dimerization in oncogenic RTKs, allosteric mutations most frequently occur at, and structurally alter, the dimerization interface. 

How are allosteric mutations oncogenic?

Allosteric mutations activate tumor drivers and inactivate tumor suppressors through the large scale conformational change.

How are allosteric mutations oncogenic in RTK?

Allosteric mutations render RTK oncogenes ligand-independent.

Consequences of Allosteric Oncogenic Mutations In EGFR AND HER2

For the ErbB RTK oncogenes, EGFR and HER2, the selectivity of the ATP site is altered in comparison to the wild type receptors. Even though there is no change in the primary sequence of the ATP site, allosteric mutant ErbB RTKs exhibit unique drug selectivity.