Delivering next-generation treatments for back of the eye disorders, with focus on diabetic eye disease

THR-149 (PKal Inhibitor)

Illustration THR-149

Mode of action

THR-149 is a plasma kallikrein (PKal) inhibitor for treatment of DME. Through the inhibition of the plasma kallikrein-kinin (PKaI-kinin) system, THR-149 prevents the induction of retinal vascular permeability, inflammation and angiogenesis. Literature data show that patients with DME have elevated levels of plasma kallikrein and that the vitreous level of plasma kallikrein varies less compared to VEGF, making it a potentially more effective target for the treatment of DME. Oxurion has enrolled the first patient in a phase I clinical study evaluating THR-149 for treatment of DME.

Oxurion is actively recruiting patients for a Phase I clinical study that is currently underway to evaluate THR-149 for the treatment of DME.

see full pipeline

Target indications

Diabetic macular edema

We are pleased to have progressed THR-149 into clinical development by initiating this Phase I study. This is a key step in assessing THR-149’s safety profile and its potential role in treating DME

- Andy De Deene, MD, Global Head of Development

Clinical trials
Phase I

Clinical study evaluating THR-149 (a PKal inhibitor) for treatment of diabetic macular edema (DME)


Ongoing, first patient enrolled

The THR-149-001 open-label, multicenter, dose escalation phase I clinical study (THR-149-001) will primarily assess the safety of a single intravitreal injection of escalating dose levels of THR-149 in patients with DME. Approximately 18 patients will be enrolled.


Initial results from the THR-149-001 study are anticipated in mid-2019.

Preclinical data

Preclinical studies on bicyclic peptide inhibitors of PKal, such as THR-149, including those published in The Journal of Medicinal Chemistry in March, have demonstrated nanomolar to picomolar potencies, and stability in biological matrices and reported prolonged retention in the eye together with in vivo efficacy in diabetic models of retinal vascular permeability. These outcomes support THR-149’s development as a possible treatment for DME and DR via a VEGF-independent mechanism of action.