- KIN001 reduced fibrotic damage of the lung in a preclinical fibrosis model
- Potential as an effective oral therapy for Idiopathic Pulmonary Fibrosis (IPF)
- Phase 2 clinical trial in IPF patients in preparation
In a mouse model of lung injury, KIN001 significantly reduced lung weights and tissue fibrosis score vs. controls. KIN001 was more effective in direct comparison to pirfenidone, a marketed IPF therapy. The combination of KIN001 with pirfenidone demonstrated greater reduction in lung fibrosis, indicating the potential for additional benefit of KIN001 in combination with the current standard of care. In order to understand the mechanisms of action of KIN001, global gene expression changes in lung tissue were measured by the RNAseq method. KIN001 significantly reduced the upregulation of multiple key inflammatory cytokines and chemokines implicated in the pathology of lung fibrosis.
“These preclinical data strongly support the potential of KIN001 to be an effective treatment for IPF and fibrotic disorders of the lung and other organs, both in single or combination therapy.” said Thierry Fumeaux, Chief Medical Officer of Kinarus. “Many patients stop therapy with the currently available drugs, due to side effects and lack of efficacy. Our data demonstrate that KIN001 possesses broad anti-inflammatory and anti-fibrotic properties which increase the probability that a patient may respond to KIN001. Together with our superior safety profile, demonstrated in clinical testing to date, this indicates that KIN001 may be more effective and better tolerated than available drugs. These data also support the potential of KIN001 to reduce severity and long-term organ damage in COVID-19.”
The Phase 2 study in IPF will be a 52-week, double-blind, randomized, placebo-controlled trial evaluating the effect of oral KIN001 on Forced Vital Capacity (FVC) in 80 patients with IPF. This study will enroll patients on current standard of care including Ofev and Esbriet. Patients not currently treated with either drug will also be included since a substantial number of patients end treatment with these two drugs due to safety concerns.
Kinarus is currently conducting a Phase 2 trial of KIN001 to treat ambulatory COVID-19 patients (“KINFAST”) with a positive SARS-CoV-2 test, which is actively recruiting in
About Idiopathic Pulmonary Fibrosis
Idiopathic pulmonary fibrosis is a devastating, progressive, irreversible, and usually lethal age-related lung disease of unknown cause. Recent evidence suggests that repeated injury to the alveolar epithelial cells plays a central role in the pathophysiology of the disease. The standard of care consists of pirfenidone (Esbriet®- Roche) or nintedanib (Ofev®-
About KIN001
KIN001 is an orally administered combination of pamapimod and pioglitazone. Pamapimod is a potent inhibitor of the p38 mitogen-activated protein kinase (MAPK), central for the cellular response in many diseases. Pioglitazone is an activator of the peroxisome proliferator-activated receptor (PPAR) gamma marketed for the treatment of type 2 diabetes. Kinarus has discovered, and patent-protected correspondingly, that the drug combination increases the efficacy and durability of therapeutic response in preclinical models reflecting various diseases with substantial unmet medical need. KIN001 is currently being developed in COVID-19, Idiopathic Pulmonary Fibrosis and wet Age-Related Macular Degeneration.
About Kinarus
For more information, please visit the company’s website at www.kinarus.com.
Contacts
Hochbergerstrasse 60C 4057 +41 61 633 29 71 info@kinarus.com | Investors & Media +41 79 367 6254 chris.maggos@cohesionbureau.com |
Legal disclaimer
THIS PRESS RELEASE DOES NOT CONSTITUTE AN OFFER TO SELL NOR AN INTIMATION TO SUBMIT A PROPOSAL FOR THE ACQUISITION OF SECURITIES OF KINARUS THERAPEUTICS HOLDING AG. THIS PRESS RELEASE IS NOT FOR RELEASE, PUBLICATION OR DISTRIBUTION, DIRECTLY OR INDIRECTLY, IN WHOLE OR IN PART, INTO OR WITHIN ANY JURISDICTION WHERE IT IS UNLAWFUL TO BE DISTRIBUTED.
Attachment
- Kinarus Preclinical IPF data (PDF)
Source:
2023 GlobeNewswire, Inc., source