We are focused on advancing the development of tecarfarin, a late-stage novel therapy with orphan drug indication for the prevention of systemic thromboembolism of cardiac origin in patients with end-stage renal disease and atrial fibrillation (ESRD + AFib).
Tecarfarin is an anticoagulation drug with the potential to replace warfarin as the standard for care for patients with ESRD + AFib.
Tecarfarin is a Phase III-ready, vitamin K antagonist (VKA), taken once a day as an oral anticoagulant like warfarin. Tecarfarin, like warfarin, was designed to have the same well-established and reversible VKA mechanism of action, but to be free of certain potentially life-threatening clearance and drug-to-drug interaction problems associated with warfarin.
Tecarfarin was developed using a retrometabolic drug design process which targets a different metabolic pathway from the one targeted by the most commonly prescribed anticoagulants. We believe this may allow elimination by large capacity and non-saturable tissue esterase pathways that exist throughout the body rather than just in the liver. Thus giving tecarfarin a better safety profile and potentially eliminates specific side effects while maintaining or improving efficacy.
In 2019, the Food & Drug Administration granted tecarfarin an Orphan Drug Designation for treating patients with end-stage renal disease and atrial fibrillation.
We are currently focused on advancing our pivotal Phase 3 trial for tecarfarin.
We believe tecarfarin has the potential to be a safer, more effective treatment option for individuals with ESRD + AFib.
Proven Safety Profile
Tecarfarin has been evaluated in 11 human clinical trials in more than a thousand individuals. In Phase 1, Phase 2 and Phase 2/3 clinical trials that have conducted thus far, tecarfarin has generally been well-tolerated in both healthy adult patients and patients with chronic kidney disease.
We have established that tecarfarin has a similar Mechanism of Action to that of warfarin, while also showing that tecarfarin’s elimination from the body was not affected by severe kidney dysfunction.
Improved Metabolic Profile
Drug metabolism refers to the process by which a drug is inactivated by the body and rendered easier to eliminate or to be cleared by the body. Most approved drugs which are prescribed for the treatment of thrombosis, are metabolized in the liver through a pathway known as the Cytochrome CYP450 system, or CYP450, by the enzymes known as CYP2C9 and CYP3A4. By using a different metabolic pathway, tecarfarin eliminates or minimizes the CYP450 metabolism in the liver.
Patients taking multiple medications, or those with impaired kidney function, can experience an overload in the pathway, creating a bottleneck that often leads to insufficient clearance, which results in a toxic build-up of one or more drugs. In some instances, patients taking multiple medications metabolized by the same CYP450 pathway may experience decreased efficacy of one or more of the medications due to rapid metabolism or increased drug effect and/or toxicity due to enzyme induction.
Our product candidate tecarfarin was designed to follow a metabolic pathway distinct from the CYP450 pathway and is metabolized by both CYP450 and non-CYP450 pathways. We believe this may allow elimination by large capacity and non-saturable tissue esterase pathways that exist throughout the body rather than just in the liver.