Q BioMed announced that together with its technology partner, Mannin Research, they are accelerating the rapid development of novel drugs for the treatment of life-threatening complications caused by COVID-19 and other viral infections. This novel drug program is being evaluated by government programs for funding and accelerated development under various COVID-19 response initiatives. Q BioMed and Mannin hope to have at least one treatment in human trials this year.
The accelerated development is the result of a joint venture between Mannin, with its Tie2 based small molecule platform that addresses vascular leakage, and Cyclica, a Toronto-based biotechnology company that has a proprietary AI-augmented drug discovery platform, Ligand Design and Ligand Express. The joint venture agreement will deploy Cyclica’s unique AI platform to accelerate the development of new treatments based on Mannin’s Tie2 based platform.
“Therapeutics based on the Tie2 platform have the potential to offer clinicians an intervention to rapidly stabilize the patient’s vascular endothelium in hospital settings, such as the intensive care unit (ICU) or emergency room (ER), when pulmonary edema is diagnosed. Such an intervention could improve outcomes without waiting for a definitive diagnosis, which has been a bottleneck in the current COVID-19 pandemic in the US and around the world,” Mannin Research CEO Dr. George N. Nikopoulos said in a company news release. “By targeting Tie2, our therapeutic may also be effective in the treatment of several conditions including pulmonary edema, ARDS and severe acute respiratory syndrome (SARS) associated with COVID-19 and the seasonal flu.”
“Simply put, drugs from Mannin’s Tie2 based platform help to stabilize ‘leaky vessels’ that play a critical part in organ injury, a major determinant of negative outcomes in patients affected by several infectious diseases, including influenza and the current COVID-19 pandemic,” Q BioMed CEO Denis Corin said in the news release. “While the COVID-19 pandemic has created an urgent need for life saving therapeutics, the Tie2 based platform addresses life threatening complications from a number of infectious diseases including inevitable future novel viral threats. We hope these treatments will be in testing in the clinic by the end of the year.”
Mr. Corin continued, “We’re also excited about the potential synergy between virus directed treatments such as remdesivir and Mannin’s host-directed therapeutics. Mannin’s therapy targets the common physiological pathways that become compromised during any viral infection. Consequently, co-administering an antiviral drug with Mannin’s therapeutic is likely to have a positive synergistic effect on the infected patient. In addition, because it is not limited to acting on a specific virus, Mannin’s therapeutic wouldn’t be affected by any viral mutation that makes the virus resistant to anti-viral.”
About Tie2 and its Mechanism of Action
Viral infections can damage the cells that make up the vessels called the endothelium. This damage leads to organ failure and allows the virus to move systemically while also increasing secondary bacterial infections. Independent research has demonstrated that reducing vascular leakage helps prevent organ failure and ameliorate acute infections.
The Tie2 receptor and its ligands, Angiopoietin 1 and 2, play an intricate role in maintaining the integrity of the vascular endothelium. This balance has a significant role in several diseases, ranging from glaucoma to infectious disease. Vascular integrity is most essential in the lung, which has the highest level of expression of Tie2 and its ligands. During infection and chronic or acute inflammation, the balance between Angiopoietin 1 and 2 is compromised to favor Angiopoietin 2, which increases vascular permeability. Activating Tie2 receptor either by restoring Angiopoietin 1 levels or through therapeutic interventions targeting its negative regulator VE-PTP has been shown to restore vascular integrity and decrease inflammation by blocking migration of NF-kB to the nucleus and blocking the expression of the adhesion integrins, VCAM1 and ICAM1.