The Program.
One molecule — VL166, a permanent, selective heparanase inhibitor — applied first where the need is sharpest.
Targeting Upstream
in Kidney Disease
Kidney disease spans many injuries — but rare kidney diseases and diabetic kidney disease (DKD) share a converging mechanism of damage in the glomerulus, the kidney's delicate filtering unit, driven by persistent inflammation and fibrosis.
Heparanase (HPSE) is a critical driver of that progression. In the kidney it destroys the glomerular basement membrane — a vital part of the filtration barrier — and triggers the pro-inflammatory and pro-fibrotic signalling that accelerates scarring.
By permanently inhibiting heparanase, VL166 works upstream of existing interventions — designed not to manage symptoms, but to halt a core molecular driver of kidney damage: protecting kidney structure and slowing progression to end-stage renal disease.
Target — heparanase (HPSE) at the glomerular basement membrane.
Mechanism — irreversible, covalent active-site inhibition.
See the mechanism →Heparanase: a hallmark of cancer
Heparanase overexpression is an established hallmark of cancer — remodelling the matrix around tumours, releasing growth factors, and promoting angiogenesis and metastasis. VL166 aims to neutralise this central mechanism.
In published work, VL166 showed efficacy across three murine models — melanoma, breast cancer and multiple myeloma — each with a significant reduction in cancer progression and metastasis.
Partnering for broader impact
As a master regulator of the cellular microenvironment, heparanase is implicated wherever chronic inflammation, tissue remodelling and fibrosis converge. We're seeking partners to explore VL166 in fibrotic disease (such as IPF or NASH), certain viral infections, and rare diseases of high unmet need.