Getting to the Core of Fibrosis

FIBROCOR WAS FOUNDED IN 2017 BY TORONTO INNOVATION ACCELERATION PARTNERS (TIAP) AND EVOTEC INT’L to develop the translational science capabilities coming from laboratories at St. Michael’s Hospital in Toronto, Canada. Leveraging a tissues biopsy collection that had been being developed for decades, Fibrocor deployed advanced technology for genetic fingerprinting and biomarkers to link clinical outcomes and to better annotate the genetic markers and biomarkers associated with fibrotic diseases. Fibrocor’s exclusive license to the tissue biorepository of kidney, liver and lung biopsies, is the core of our discovery engine. The platform is further differentiated by its best-in-class longitudinal medical record data associated with the samples.

As the new President and CEO of Fibrocor Therapeutics, William P. Newsome III is enthusiastic about the future, and with good reason. Newsome and his management team have a combined industry experience of nearly 150 years. They are backed by an experienced and active board and complemented with world-class drug hunting experts that leverage their vast networks and knowledge base. This positions Fibrocor to be a leading player in attacking fibrosis head-on.

WHAT PART DOES FIBROCOR THERAPEUTICS PLAY IN TARGETING FIBROTIC DISEASES?

Pathological fibrosis is the scarring or disruption of tissue caused by a persistent tissue repair response (myofibroblast activation) resulting in the excessive accumulation of extracellular matrix (ECM) components that can ultimately lead to organ failure.

Fibrosis underlies many severe diseases with poor prognosis and no approved therapies. These diseases affect the kidneys, pancreas, heart, liver, lungs, eyes and skin.

Nearly 45% of all deaths in the developed world are attributed to some type of chronic fibroproliferative disease.

Fibrocor seeks to treat the unmet medical needs of fibrosis. Our platform enables systematic discovery of novel fibrosis targets by dissecting shared and unique fibrosis pathways and targets across fibrotic diseases. By marrying extensive longitudinal human biobank data with next generation sequencing tools to uncover clinically validated fibrotic disease targets, Fibrocor discovers and develops highly effective therapies for fibrosis. A breakthrough in any single indication can lead to several others resulting in a “pipeline in a product.”

Using patient samples to derive and validate fibrogenic targets means our platform enables systematic discovery of novel fibrosis targets. By linking transcriptional markers to patient outcomes, the Fibrocor drug discovery platform identifies fibrosis-related targets and develops therapeutic programs from the validated targets.

WHAT CAN YOU TELL US ABOUT YOUR PIPELINE?

Fibrocor’s best-in-class target ID and selection process has delivered a growing portfolio of first or best-in-class fibrosis programs. The pipeline consists of three at or near pre-clinical candidate (PCC) stage programs that have been prioritized from a large pool of novel fibrosis-related targets. The small molecule programs include: a lead program (FIB992), an exquisitely selective kinase inhibitor at pre-clinical candidate stage (PCC) that is indicated for idiopathic pulmonary fibrosis (IPF)-lead indication, Alport Syndrome, (AS)and Chronic Allograft Nephropathy (CAN). The second small molecule program (FIB991) is in late lead optimization (LO) stage (6-12 mo from PCC) that is indicated for IPF, chronic kidney disease (CKD), other fibrotic diseases. In addition, we have a monoclonal antibody (mab) program (FIB918), a collagen binding integrin mAb at PCC stage, indications include: Alport Syndrome, (AS)= lead indication, CAN, Primary Sclerosing Cholangitis (PSC) Primary Biliary Cholangitis (PBC). The biorepository still has remarkable untapped potential, however our current, short-term focus is all hands onboard to drive the existing programs into the clinic.

Pathological fibrosis is the scarring or disruption of tissue caused by a persistent tissue repair response (myofibroblast activation) resulting in the excessive accumulation of extracellular matrix (ECM) components that can ultimately lead to organ failure.
Pathological fibrosis is the scarring or disruption of tissue caused by a persistent tissue repair response (myofibroblast activation) resulting in the excessive accumulation of extracellular matrix (ECM) components that can ultimately lead to organ failure.

WHAT’S THE STRATEGY TO MOVE THE PROGRAMS FORWARD?

FIB992 is our lead program. Fibrocor is seeking Series A financing in 2023 to advance 992 to phase 2 clinical trials. IND Q4 2023 and initiate Phase I in H1/ 2024

FIB991 will reach PCC later this year and complete IND studies Q1 2024.

FIB918 is in active partnering discussions to fund FIB918 to ph1b in Alport Syndrome with phase 1 studies beginning in 2025. Additional indications include acute kidney injury, CAN, PSC and PBC.

THIS IS AN ASTONISHING AMOUNT OF INNOVATION AND PROGRESS IN A RELATIVELY SHORT PERIOD OF TIME. HOW HAVE YOU MANAGED TO ACCOMPLISH THIS AND STAY LEAN AS AN ORGANIZATION?

Fibrocor is rooted in strong translational sciences tied to human patient samples and disease progression, we started by choosing the right targets. Then rather than building out extensive labs and investing heavily in capital equipment and a large footprint and internal team, we kept our internal operations to core capabilities and partnered with world class organization like Evotec Int’l and IONTIS- FairJourney for integrated program support. This approach has led to a capital efficient model that has allowed us to advance nimbly and efficiently. The company has a modest valuation based on our current pipeline and the untapped potential of the biorepository, this is another significant
differentiator that appeals to partners and investors.

Current investors include BioGeneration Ventures (BGV), Galapagos, Evotec Int’l and TIAP. Fibrocor is currently seeking collaboration partners and investors interesting in leading or participating in our Series A financing round. Please contact: [email protected]

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