Melbourne – October 4, 2026 -- CSL and Alentis Therapeutics have signed an exclusive global collaboration to develop and commercialize lixudebart, a potential first-in-class therapy targeting claudin-1 for rare kidney and liver diseases, with CSL paying Alentis US$355 million upfront and up to US$1.2 billion in commercial milestones.

CSL pays $355 million upfront, commits $1.2 billion in milestone payments

Under the agreement, CSL will fully fund the ongoing Phase 2 RENAL trial, the planned Phase 3 trial in ANCA-associated vasculitis with rapidly progressive glomerulonephritis (AAV-RPGN), and Phase 2 trials in focal segmental glomerulosclerosis (FSGS) and primary sclerosing cholangitis (PSC). Once commercialized, global profits will be split 55 percent to CSL and 45 percent to Alentis.

Lixudebart shows kidney and liver function improvements in early trials

In an interim analysis of 26 AAV-RPGN patients in the Phase 2 RENAL trial, lixudebart showed improvement in kidney function measured by eGFR and proteinuria at 24 weeks. In a Phase 1b trial of 41 patients with advanced F3/F4 liver fibrosis, the drug demonstrated improved liver function at six weeks, with dose-dependent claudin-1 target engagement in both studies. The FDA has granted lixudebart Orphan Drug designation for idiopathic pulmonary fibrosis.

Partnership pairs Alentis science with CSL's nephrology commercialization network

Alentis CEO Dr Mark Pruzanski said the deal allows parallel acceleration of lixudebart development across multiple indications and validates claudin-1 as a therapeutic target for the company's broader pipeline. CSL's EVP and Head of R&D, Dr Bill Mezzanotte, said the companies aim to address AAV-RPGN patients who face rapid, often irreversible kidney function decline despite current immunosuppressive treatments, while also pursuing potential benefit in FSGS and PSC.

Deal extends CSL's nephrology franchise into novel fibrosis mechanisms

AAV-RPGN causes rapid loss of kidney function over days to weeks, with most patients developing significant or total kidney function loss despite potent immunosuppressive therapy. Lixudebart's mechanism targets exposed claudin-1, a driver of inflammatory and fibrotic signaling implicated across kidney, liver, lung and intestinal diseases.