Galytx targets galectin-3, a central mediator of fibrosis, inflammation and tumour progression across high unmet need diseases. Our programmes are focused on biologically defined populations where galectin-3 modulation can alter disease trajectory.

The Clinical Challenge

Heart Failure with Preserved Ejection Fraction (HFpEF) accounts for approximately half of all heart failure cases and continues to rise in prevalence globally. Despite its growing burden, there are currently no therapies that directly modify the underlying structural disease process.


HFpEF is increasingly recognised as a biologically defined condition characterised by progressive myocardial fibrosis and inflammatory activation, leading to ventricular stiffening and impaired cardiac function.

The Clinical Challenge

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype associated with early metastasis, high relapse rates, and limited targeted treatment options. It disproportionately affects younger women and remains an area of high unmet clinical need.


Galectin-3 plays a central role in tumour progression, metastasis and therapeutic resistance in TNBC, making it a compelling target for intervention.

One Target. Multiple Disease Pathways.

Galytx is advancing galectin-3 inhibitors across fibrosis-driven cardiovascular disease and aggressive oncology indications.

Explore Our Platform

DISEASE FOCUS- HFpEF

Modulating the

Fibrosis–Inflammation Axis in HFpEF

Heart Failure with Preserved Ejection Fraction (HFpEF) accounts for approximately half of all heart failure cases and continues to rise globally. Despite its scale, there are currently no therapies that directly modify the structural drivers of disease progression.



Galytx is targeting galectin-3 as a central regulator of fibrosis and inflammatory remodelling in biologically defined HFpEF populations.

The Biological Rationale

HFpEF is increasingly recognised as a condition characterised by progressive myocardial fibrosis and chronic low-grade inflammation. This fibrosis–inflammation axis contributes directly to ventricular stiffening, impaired diastolic relaxation and adverse structural remodelling.

Galectin-3 plays a regulatory role in macrophage activation, fibroblast signalling and extracellular matrix deposition. Elevated levels are associated with fibrotic activity and adverse cardiovascular outcomes.

Development Strategy

The Galytx HFpEF programme is built around:

  • Biomarker-defined patient stratification
  • MRI-based structural remodelling endpoints
  • Circulating fibrosis biomarker assessment
  • A clinical-stage oral small-molecule inhibitor (GXR1) with established human safety

This imaging- and biomarker-guided approach is designed to enable rapid proof-of-concept in fibrosis-driven disease.

DISEASE FOCUS - TNBC

Targeting Galectin-3 in Triple-Negative Breast Cancer

Triple-negative breast cancer (TNBC) is an aggressive subtype characterised by early metastasis, high relapse rates and limited targeted treatment options. It disproportionately affects younger women and remains an area of significant unmet need.



Galytx is developing galectin-3 inhibitors to address tumour progression and therapeutic resistance in TNBC.

Mechanistic Rationale

Galectin-3 contributes to multiple stages of TNBC development, progression and metastasis, including tumour growth, metastatic dissemination and resistance to chemotherapy. It also shapes the tumour microenvironment and suppresses anti-tumour immune responses.

High tumour and circulating galectin-3 levels are associated with poorer prognosis and increased metastatic potential.

Therapeutic Strategy

The Galytx TNBC programme includes:

  • Novel galectin-3 inhibitors with strong in vitro and in vivo evidence
  • A repurposed asset with an established safety profile


  • Dual potential benefit:
  • Direct tumour suppression
  • Sensitisation to cytotoxic and immune-based therapies



By targeting a central regulator of tumour biology, Galytx aims to introduce a mechanistically differentiated strategy for durable TNBC treatment.