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OUR SCIENCE

A Smarter Model For Cancer Therapy.

At Jabez, our “3-C model” guides how we select, advance, and deliver our growing pipeline of cancer therapeutics.

OUR “3-C” THERAPEUTICS MODEL

Our Therapeutics Are

At Jabez, we identify and advance cancer therapeutics that are easy to take, easy to make, and ready to combine, not recreate.

“3-C” Cancer Therapeutics are:

Convenient

Designed for ease of use; oral administration, well-tolerated profiles, and outpatient compatibility when possible.

Cost-Effective

Synthesized with scalable, tractable chemistry. Built for real-world manufacturing, storage, and distribution.

Cooperative (Synergistic)

Mechanistically synergistic with existing standards of care. We prioritize biological rationale, not empirical stacking.

We’re not redefining biology – we’re leveraging it better.

OUR APPROACH

A Biology-First Approach

We do not rely on trial-and-error combinations. We apply rigorous mechanistic reasoning to identify rationale, biological synergy up front.

Step #1

Identification & Licensing

We identify and license promising molecules with well-characterized mechanisms that align with our 3-C model and strategic synergy criteria.

Step #2

Validation & Planning

We design targeted development plans choosing the precise combinations, and patient populations to maximize impact.

Step #3

Clinical Deployment

We execute focused, efficient trials, bringing the right therapy to the right patients with precision, speed, and intent.

JBZ-001:

Our Lead Compound

JBZ-001 is an oral DHODH inhibitor currently in a Phase 1 clinical trial for advanced solid tumors and non-Hodgkin lymphoma.

It brilliantly exemplifies our 3-C model: 

  • Convenient: Well-tolerated, oral small molecule
  • Cost-Effective: Leverages Nobel Prize-winning, scalable chemistry 
  • Cooperative: Displays potent synergy with well-established treatment regimens.

JBZ-001: Small Molecule DHODH Inhibitor

DHODH, JBZ-001 & Cancer

To understand how JBZ-001 fights cancer, it is important to first understand the role of DHODH. Put simply, DHODH is an enzyme that is crucial for the production of pyrimidine nucleotides – essential factors in the creation of new DNA and RNA, and vital for cell division. 

Cancer cells have a very high dependence on DHODH for their survival and growth – much higher than healthy cells – and therefore are very sensitive to the loss of DHODH function. So, by binding to and inhibiting DHODH, JBZ-001 selectively targets and kills cancer cells.

OUR SYNERGISTIC THERAPEUTIC APPROACH

JBZ-001's Synergistic Potential

While JBZ-001 shows strong single-agent activity, preclinical studies have revealed two remarkable mechanisms of synergy with standard treatments in two key cancer types.

Acute Myeloid Leukemia (AML)

Enhancing AML Treatment

JBZ-001 promotes myeloid cell differentiation and has demonstrated a potent ability to enhance the activity of several AML-specific therapeutics across AML subtypes. 

CD38 Antibodies (mAbs)

Increase Activity of CD38 mAbs

In both AML and multiple myeloma models, JBZ-001 increases surface expression of CD38 on tumor cells – dramatically enhancing anti-cancer activity of CD38-targeting antibodies.