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Oxford Finance Closes $20MM Debt Facility With Inhibrx

April 10, 2015, 07:07 AM
Filed Under: Medical

Oxford Finance LLC, a specialty finance firm that provides senior debt to life sciences and healthcare services companies, announced the closing of a $20 million senior secured term loan agreement with Inhibrx, a biologic immunotherapeutic company focused on the treatment of unmet medical needs in oncology, infectious disease and inflammatory conditions. Proceeds of the loan will enable Inhibrx to continue to advance its extensive portfolio of therapeutics.

"We are pleased to provide financing to Inhibrx to support the development of their therapeutic pipeline addressing various clinical targets," said Christopher A. Herr, managing director for Oxford Finance. "The company currently has a promising licensing agreement with a major biopharmaceutical company for one of its assets, and has a unique business model that enables a cost effective and accelerated process for advancing other therapeutics into the clinic."

"We appreciate Oxford's support of our efforts to develop innovative therapeutics for patients in need of better treatment options," said Mark Lappe, chief executive officer of Inhibrx.

Oxford Finance is a specialty finance firm providing senior secured loans to public and private life sciences and healthcare services companies worldwide. For over 20 years, Oxford has delivered flexible financing solutions to its clients, enabling these companies to maximize their equity by leveraging their assets. In recent years, Oxford has originated over $2 billion in loans, with lines of credit ranging from $500 thousand to $75 million. Oxford is headquartered in Alexandria, Virginia, with additional offices in California, Massachusetts and North Carolina.
About Inhibrx

Inhibrx is a biologic immunotherapeutic company focused on the treatment of unmet medical needs. Inhibrx's proprietary platforms enable fit-for-function biotherapeutics that optimally interface with the biology of each target antigen, focus immune activation and mediate enhanced signaling.

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