BridgeBio Pharma is building a war chest for its showdown with Pfizer. Facing a deep-pocketed rival, the biotech has struck a set of financing deals worth up to $1.25 billion to support an anticipated launch and a schedule of phase 3 readouts for other assets.
Last year, BridgeBio raised $250 million by selling stock, enabling it to exit the third quarter with more than $500 million in the bank. But with winning heart disease market share from Pfizer high on its to-do list—and the roadmap for the coming years featuring multiple late-stage readouts—the biotech has decided it needs to stockpile more cash.
Blue Owl Capital and Canada Pension Plan Investment Board have met that need. BridgeBio is set to get $500 million, in total, from the two companies upon FDA approval of acoramidis. In return, the investors will receive 5% royalties on worldwide net sales of the molecule and stand to pocket up to $950 million, a 1.9-time return on their investment. The deal features a provision for if BridgeBio is acquired.
BridgeBio also refinanced its existing senior credit facility. The agreement with Blue Owl will give the biotech $450 million, extend the maturity of its loan from 2026 to 2029 and grant it access to a further $300 million “to support strategic corporate development activities.”
The first priority is to bring acoramidis to market in transthyretin amyloid cardiomyopathy (ATTR-CM), an indication currently served by Pfizer’s tafamidis products. BridgeBio filed for FDA approval in November, putting it on course to bring the product to the U.S. market in the second half of 2024. Submissions for approval in other markets are also planned (PDF) for this year.
While analysts have warned Pfizer is “quite entrenched” and “might be difficult to displace,” ATTR-CM is a large, growing market and BridgeBio foresees “billions of peak year sales” for acoramidis. The revenue, plus the biotech’s existing cash, will support the development of a clutch of other candidates. BridgeBio is running phase 3 trials in achondroplasia, a form of muscular dystrophy and the calcium disorder ADH1.