Dr. Steffen-Sebastian Bolz establishes a new transfection model in resistance arteries, demonstrating the role of the signaling molecule, sphingosine-1-phosphate (S1P), as a strong vasoconstrictor involved in the myogenic mechanism. Dr. Darcy Lidington joins research group and starts early collaborative work.

Dr. Bolz is offered the opportunity to establish a microvascular lab at the University of Toronto. The team continues research on S1P signaling in the regulation of tone in resistance arteries, later expanding work into mouse disease models, including hearing loss.  

To enable further use of genetic models, the lab establishes methods to look at distinct microvascular beds in the the cerebral and skeletal microcirculation.

Dr. Bolz becomes founding Director of the Centre for Microvascular Medicine (CMM) and increases cross-disciplinary collaboration in the field, integrating circadian aspects, heart failure models, and research targeting peripheral resistance.

Alexandra Papaelias joins CMM as the centre's coordinator to foster public-private partnerships supporting research translation and commercialization in the network.

A series of Toronto research collaborations in models of diabetes, heart failure and subarachnoid hemorrhage further define aspects driving increases in vessel tone in cerebral and peripheral microcirculation.

The team identifies CFTR as a critical regulator of S1P signaling in diseases involving TNFα, a common inflammatory marker.

An angel investor joins the team to fund the translation of core discoveries with clinical applications.

Two patent families related to molecular signalling in the cerebral and peripheral microvasculature are filed and an early fundraising package is built to develop clinical interventions for hypertension, stroke and heart failure.

Dr. Lidington and CMM collaborators publish pre-clinical findings in JACC: Basic to Translational Science demonstrating the key role of CFTR in regulating cerebral artery tone, with research showing beneficial effects in experimental disease models with commercially available CFTR-correctors.

Following successful Series A, Qanatpharma AG is founded in Switzerland as the company’s corporate headquarters under the direction of Christian Albrecht (CEO) Gunter Jucho (CFO) and Steffen-Sebastian (CSO and CMO).

QP receives Orphan Drug Designation (ODD) for therapeutic treatment of SAH using CFTR-correctors from the European Medicines Agency and the US Food and Drug Administration.

QP's screening platform identifies several peripheral targets and drug candidates for pre-clinical testing. QP formalizes research collaboration with the University of Toronto to carry out the validation studies in vessels and animal models on-site in downtown Toronto.

With clinical collaborators at the University-Hospital network, QP designs the LYRIC Trials to clinically test CFTR-correctors in patients with heart failure and subarachnoid hemorrhage using MRI imaging and questionnaires testing cognitive abilities.

Qanatpharma Canada Ltd. is founded in Toronto as the company’s primary hub for QP’s research program, spanning the entire continuum from target identification and validation, drug discovery and development to clinical trials.

QP initiates drug development with manufacturing partner to repurpose a commercial CFTR-corrector, lumacaftor, for clinical testing.

QP completes Phase 1 clinical trial to assess the bioequivalence and food effect bioavailability of Lumacaftor (NCT05968612).

The Phase 2 proof-of-concept trial, LYRIC-HF investigates the effectiveness of the drug lumacaftor to restore cerebral blood flow autoregulation and curb cognitive decline in heart failure patients.

With an expanding scientific team, QP builds core expertise in AI and machine-learning approaches to integrate in-silico strategies in its drug discovery pipeline that focus on the next generation of microvascular treatments (GENESiS-SAH, GENESiS-HF, RESiST-HF).