Developing next generation treatments to preserve vision for patients with diseases affecting the back of the eye

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 treating DME. Oxurion has reported positive topline phase 1 results for the clinical study evaluating THR-149 for the treatment of DME.

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Target indications

Diabetic macular edema

"The immediate onset of action and the duration of the BCVA improvement following 1 injection of THR 149 are impressive. Mean CST findings are within variability of measurement. Macular Volume correlates with reported BCVA improvement, potentially offering a new anatomical predictor for BCVA improvement."

- Pravin Dugel, MD -  Read full presentation

Clinical trials
Phase I

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


Preparing to initiate phase 2 after positive results for phase 1.

The THR-149-001 open-label, multicenter, dose escalation phase 1 clinical study (THR-149-001) assesses the safety of a single intravitreal injection of escalating dose levels of THR-149 in patients with DME. A total of 12 patients have been recruited.


Oxurion reports two sets of positive topline data for phase 1.

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.