Sanofi and Merck to conduct phase 2 trial of THOR-707 in combo with Keytruda

Sanofi has entered into an agreement with Merck & Co., Inc., Kenilworth, NJ, USA (known as MSD outside the US and Canada) to conduct a phase 2 clinical trial to evaluate the safety, pharmacokinetics, and preliminary efficacy of THOR-707, a highly differentiated non-alpha IL-2 candidate with a best-in-class profile, combined with or in sequenced administration with MSD’s Keytruda (pembrolizumab) in patients with various cancers.

Under the agreement, Sanofi will sponsor the clinical trials while MSD will provide Keytruda. THOR-707 is currently being evaluated by Sanofi in an ongoing phase 1 open-label, multi-center, dose escalation and expansion trial.  This study is designed to evaluate the safety and tolerability of THOR-707, and to determine its recommended phase 2 dose alone and in combination with anti-PD-1 and anti-EGFR antibodies.

In addition to testing THOR-707 in combination with Keytruda, Sanofi is separately evaluating the activity of this novel biologic in combination with other anti-PD-1 antibodies, including Libtayo (cemiplimab-rwlc) and with anti-EGFR and anti-CD38 antibodies for various types of cancer tumors.

THOR-707 demonstrated in preclinical studies the ability to induce the expansion of CD8+T-cells resulting in anti-tumor effects both as single agent as well as in combination with an anti-PD1 mAb.

It is the first molecule from the Synthorin platform, Sanofi’s unique expanded genetic alphabet platform, which has the potential to create a new generation of precision medicines for oncology and autoimmune disease.

About THOR-707

THOR-707 has the potential to be a best-in-class IL-2 therapeutic for the treatment of many types of malignancies and may demonstrate improved pharmacology allowing for less frequent dosing. In pre-clinical experiments, THOR-707 shows striking synergy with anti-PD-1 therapeutics.

It is a precisely PEGylated engineered version of interleukin-2 (IL-2), where the PEG chain is attached at a location on IL-2 that prevents it from binding to immune receptors that cause drug toxicities (IL-2R-alpha, CD25) while preserving binding to immune receptors that selectively expand tumor-killing T effector and Natural Killer (NK) cells without the immunosuppressive effects of regulatory T cells or vascular leak syndrome (VLS) inducing eosinophils.