R1 Therapeutics licenses Alebund’s pan-phosphate transporter inhibitor alongside Series A launch

R1 Therapeutics, a newly formed clinical-stage company, has licensed exclusive rights to develop and commercialize Alebund Pharmaceuticals’ AP306 outside Greater China under a collaboration and license agreement announced March 17, 2026. AP306 is a first-in-class pan-phosphate transporter inhibitor in development for hyperphosphatemia in patients with chronic kidney disease on dialysis. Shanghai-based Alebund retains all rights in Greater China.

The licensing deal comes alongside’s R1 Therapeutics’ official launch following an oversubscribed USD 77.5 million Series A financing announced on the same day. The financing was co-led by Abingworth, DaVita Venture Group, and F-Prime, with participation from Curie.Bio, SymBiosis, and US Renal Care.

Under the license deal, the aggregate financial terms include development, regulatory, and commercial milestone payments of up to low triple-digit millions of US dollars, specifics not disclosed. Alebund will receive tiered royalties in the low double-digit percentage range on net sales of AP306 in R1’s territory. Alebund will also receive a non-dilutive equity interest in R1, with the right to participate in future commercial upside through dividends. R1 will fund and lead global clinical development, with Alebund serving as a collaborative development partner. A global Phase IIb multi-regional clinical trial in the US and China is planned to initiate later in 2026.

The deal context

AP306 is a small molecule originally discovered by Chugai Pharmaceutical and subsequently licensed to Alebund in a 2021 deal. The compound inhibits three intestinal phosphate transporters — NaPi-IIb, PiT-1, and PiT-2 — that mediate active phosphate absorption in the gastrointestinal tract. In patients with chronic kidney disease on dialysis, impaired renal phosphate excretion leads to hyperphosphatemia, a condition associated with vascular calcification and cardiovascular complications. Current standard-of-care phosphate binders require patients to take multiple large pills with each meal, and adherence remains poor. AP306 targets the transcellular absorption pathway directly rather than binding phosphate in the gut lumen, representing a distinct pharmacological approach to hyperphosphatemia treatment in CKD.

Alebund completed a Phase IIa trial in hemodialysis patients that demonstrated reductions in serum phosphorus with acceptable safety and tolerability. Results were published in Kidney International Reportspublication) and presented at the 61st European Renal Association Annual Congress). A Phase I ADME study in healthy subjects is also ongoing).

The Alebund-R1 collaboration positions AP306 as R1’s lead program. R1’s investor syndicate includes DaVita, which serves approximately 295,000 patients across more than 3,200 dialysis centers globally, and US Renal Care, the largest privately held dialysis provider in the United States. Their involvement as both investors and kidney care providers could facilitate clinical trial enrollment and eventual commercial access. Alebund maintains a broader renal pipeline that includes AP301, an oral phosphate binder in global Phase III, and AP303, a dual PPAR agonist with US FDA Orphan Drug Designation for autosomal dominant polycystic kidney disease.

The AP306 chronic kidney disease program enters a competitive landscape where Ardelyx’s tenapanor (XPHOZAH), an NHE3 inhibitor that blocks paracellular phosphate transport, is the only approved non-binder therapy for hyperphosphatemia in dialysis patients. Two earlier NaPi-IIb-selective inhibitors — Daiichi Sankyo’s DS-2330b and Astellas’ ASP3325 — failed to show adequate clinical efficacy, which may reflect the limitations of targeting a single transporter rather than all three.

AP306’s pan-transporter inhibition is designed to prevent compensatory upregulation of untargeted transporters, a mechanism that may have contributed to the failure of single-target approaches. The planned Phase IIb trial will need to confirm whether this broader inhibition profile translates into clinically meaningful phosphate reduction beyond what existing therapies achieve.