GSK closing in on USD 950m purchase of 35Pharma for pulmonary hypertension drug

UK giant GSK plc revealed the signing of an agreement to acquire privately held Canadian biotech 35Pharma for USD 950 million in cash, focused on the latter’s investigational pulmonary hypertension asset HS235. The Phase I stage HS235 is an activin receptor signaling inhibitor that is being prepared for studies in pulmonary arterial hypertension (PAH) and pulmonary hypertension due to heart failure with preserved ejection fraction (PH-HFpEF).

The transaction will see GSK acquire 100% of 35Pharma’s equity and is subject to customary regulatory approvals in the US and Canada, including review under the Hart-Scott-Rodino Act and the Competition Act.

HS235 targeting validated activin pathway

GSK’s acquisition positions HS235 within a rapidly evolving competitive landscape defined by the 2024 approval of Merck & Co.’s sotatercept (Winrevair), currently the only marketed activin-pathway therapy for PAH.

Winrevair has demonstrated that targeting activin signaling can modify underlying pulmonary vascular disease biology rather than primarily addressing vasoconstriction — the mechanism of action of most legacy PH therapies such as endothelin receptor antagonists and phosphodiesterase-5 inhibitors.

However, sotatercept’s clinical use has been associated with adverse effects including bleeding and telangiectasia, which are thought to be related in part to ligand binding across the broader BMP9/10 signaling axis.

HS235 has been engineered with enhanced selectivity designed to reduce interaction with BMP9 and BMP10 ligands, potentially addressing a tolerability limitation of first-generation activin pathway inhibitors.

GSK has indicated that this selectivity may lower bleeding risk — a clinically relevant consideration in PH populations where a substantial proportion of patients require concomitant anticoagulant or antiplatelet therapy.

Potential differentiation beyond hemodynamics

In addition to pulmonary vascular effects, early clinical studies cited by 35Pharma suggest HS235 may produce dose-dependent reductions in visceral fat mass while preserving lean mass and improving insulin sensitivity. Such metabolic effects could be relevant in PH-HFpEF populations, where obesity and insulin resistance are common comorbidities that contribute to disease progression and may not be directly addressed by current therapies. Preclinical studies have also suggested improvements in cardiac function in obesity-associated HFpEF models.

Pulmonary hypertension remains a progressive cardiopulmonary disorder affecting more than 80 million people worldwide across multiple etiologies, with limited treatment options and an estimated five-year survival rate of approximately 50%. Activin signaling inhibitors are expected to account for a growing share of the PH therapeutic market, forecast to reach USD 18 billion by 2032.