Ardelyx, Inc. (Nasdaq: ARDX) announced on 5/22/18 the pricing of an underwritten public offering of 12,500,000 shares of its common stock at a public offering price of $4.00 per share, before underwriting discounts and commissions, for gross proceeds of $50,000,000. In addition, the Company has granted the underwriters of the offering the right for a period of 30 days to purchase up to an additional 1,875,000 shares of common stock at the public offering price, less underwriting discounts and commissions.
The company intends to use the proceeds to support its clinical development and pre-commercialization efforts for tenapanor for the treatment of hyperphosphatemia in patients with end-stage renal disease who are on dialysis. Tenapanor is currently in second phase 3 clinical trials for hyperphosphatemia.
Ardelyx also intends to use some of the money to support the research needed to submit an NDA for tenapanor for irritable bowel syndrome with constipation and for general corporate purposes and working capital. It was announced in October of 2017 that tenapanor had hit all primary and secondary endpoints in a phase III study for IBS-C.
Tenapanor, invented and developed by scientists at Ardelyx, is a first-in-class, proprietary, minimally absorbed, oral, experimental medication in late-stage clinical development. It has a unique mechanism of action that, in IBS-C, acts by inhibiting, or blocking, the NHE3 transporter in the gastrointestinal (GI) tract to reduce the absorption of dietary sodium. Blocking NHE3 results in an increase in the amount of sodium in the gut. This increased sodium in the gut leads to an increase of fluid in the gut, loosening stool and helping to relieve constipation. There has also been a desired benefit in the abdominal pain component of IBS-C in the studies to-date.
In hyperphosphatemia, tenapanor blocks the NHE3 sodium transporter in the GI tract, reducing the absorption of dietary sodium and resulting in increased protons within the cells. The increase in protons causes a preferential reduction in phosphate uptake by tightening junctions or pores that regulate phosphate absorption in the GI tract
