Cereno Scientific's novel HDACi CS014 has potential to become an effective antithrombotic therapy in patients with a high risk of thrombotic events as presented at the ASH Meeting

The study presented at the ASH Annual Meeting sought to determine if CS014, histone deacetylase (HDAC) inhibitor, either alone or in combination with the FXa inhibitor rivaroxaban, is able to effectively inhibit platelet and fibrin-rich thrombosis formation at the site of vascular injury without causing a significant increase in the bleeding risk in a mouse cremaster thrombosis model. The findings suggest that while CS014 and rivaroxaban are each effective antithrombotic agents, they work well together to minimize clot formation and CS014 in combination did not alter coagulation compared to rivaroxaban alone. Hence, CS014 has the potential to enrich the toolbox of antithrombotic therapies to prevent thrombosis without bleeding in patients with a high risk of thrombotic events.

 

“Globally, there is a high occurrence of platelet-rich thrombotic clots. These patients are commonly treated with a combination of therapies, to prevent occlusive thrombotic events which, however, can increase the risk of bleeding. Here we show that, when used together with rivaroxaban, CS014 is able to inhibit platelet and fibrin-rich thrombosis formation without an increase in the risk of bleeding,” said Sten R. Sörensen, CEO, Cereno Scientific.

 

Drug candidate CS014 is a novel HDAC inhibitor in development as a treatment for arterial and venous thrombosis prevention. Preparations are currently ongoing towards a Phase I study and include completion of the preclinical development program, including a preclinical safety program that has already been completed, development and manufacturing of the investigational formulation used for oral dosing of the healthy volunteers and obtaining permission from the Swedish Medical Products Agency as well as the Ethics Committee to start the study. The Phase I study is estimated to be initiated in Sweden during the first half of 2024.

 

The abstract presented at the 65th ASH Annual Meeting & Exposition is titled “HDAC Inhibitor CS014 Attenuates Thrombosis Alone and in Combination with Rivaroxaban without Increased Risk of Bleeding”, was authored by L. Stanger, M. Holinstat, S. Lambert and P. Yalavarthi at the Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI, US; B. Dahlöf and, N. Bergh at the University of Gothenburg, Gothenburg, Sweden. The abstract will be presented by Dr. Michael Holinstat, lead of Cereno’s development programs at the University of Michigan and Director of Translational Research at Cereno. The abstract can be found here: https://ash.confex.com/ash/2023/webprogram/Paper186602.html

 

 

 

For further information, please contact:

Tove Bergenholt, Director IR & Communications
Email: tove.bergenholt@cerenoscientific.com
Phone: +46 732-366 246

Sten R. Sörensen, CEO
Email: sten.sorensen@cerenoscientific.com
Phone: +46 73-374 03 74

About CS014

The investigational drug CS014 is a histone deacetylase inhibitor (HDACi) in development as a treatment for arterial and venous thrombosis prevention. This innovative drug candidate represents a groundbreaking approach to antithrombotic treatment potentially without the associated increased risk of bleeding in humans. The drug candidate CS014 is a new chemical entity with a multi-fold mechanism of action as an epigenetic modulator – regulating platelet activity, fibrinolysis, and clot stability for the prevention of thrombosis without increased risk of bleeding. In preclinical studies, CS014 demonstrates inhibition of clot formation following vascular injury by significantly attenuating platelet activation and reducing fibrin formation at the injury site. CS014 potentially offers a significantly lower risk of bleeding compared to other antithrombotic therapy, as validated in preclinical studies. CS014’s safety and tolerability will be further assessed in the Phase I study planned to be initiated in H1 2024.

About Cereno Scientific AB

Cereno Scientific develops innovative treatments for common and rare cardiovascular disease. The lead drug candidate, CS1, is a HDAC (histone deacetylase) inhibitor that acts as an epigenetic modulator with pressure-reducing, reverse-remodeling, anti-inflammatory, anti-fibrotic and anti-thrombotic properties. A Phase II study is ongoing to evaluate CS1’s safety, tolerability, and efficacy in patients with the rare disease pulmonary arterial hypertension (PAH). A collaboration agreement with global healthcare company Abbott allows Cereno to use their cutting-edge technology CardioMEMS HF System in the study. Two initiatives performed during the ongoing Phase II study have shown positive findings suggesting the potential clinical benefit of CS1 in PAH patients. These initial findings are, however, not a guarantee of the final study results that are expected in Q2 2024. Cereno also has two promising preclinical drug candidates in development through research collaborations with the University of Michigan. Investigational drug CS014 is a HDAC inhibitor in development as a treatment for arterial and venous thrombosis prevention. The innovative drug candidate represents a groundbreaking approach to antithrombotic treatment potentially without the associated increased risk of bleeding in humans. CS014 is a new chemical entity with a multi-fold mechanism of action as an epigenetic modulator – regulating platelet activity, fibrinolysis, and clot stability for the prevention of thrombosis without increased risk of bleeding as documented in preclinical studies. Drug candidate CS585 is a prostacyclin receptor agonist that has been documented in preclinical studies to target the IP receptor for prevention of thrombosis without increased risk of bleeding. The company is headquartered in Gothenburg, Sweden, and has a US subsidiary Cereno Scientific Inc. based in Kendall Square in Boston, Massachusetts, US. Cereno is listed on the Nasdaq First North (CRNO B). More information on www.cerenoscientific.com.

 

Datum 2023-12-13, kl 09:10
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