Cereno Scientific Announces First Peer-Reviewed Publication on HDAC Inhibitor CS014: Antithrombotic Efficacy Without Bleeding Risk Supports Broad Potential in Cardiopulmonary Diseases
Rhea-AI Summary
Cereno Scientific (NASDAQ First North: B) announced a peer-reviewed publication (Journal of Thrombosis and Haemostasis) on CS014, a novel HDAC inhibitor engineered to improve upon valproic acid by reducing hepatotoxic 4-ene metabolite formation while preserving HDAC activity. The manuscript reports potent antithrombotic effects across small artery, large artery and large vein models achieved at doses that preserve normal coagulation and bleeding time. Cereno also reported positive Phase I safety and tolerability at exposures predicted to support efficacy and said it is preparing for Phase II with initial focus on idiopathic pulmonary fibrosis.
Positive
- Peer-reviewed publication validating CS014 mechanism and nonclinical pharmacology
- Antithrombotic efficacy in small artery, large artery and large vein models
- Maintains normal coagulation and bleeding time at efficacious doses
- Produces substantially lower 4-ene hepatotoxic metabolite versus VPA
- Positive Phase I safety and tolerability at predicted efficacious exposures
Negative
- None.
News Market Reaction
On the day this news was published, B gained 0.48%, reflecting a mild positive market reaction.
Data tracked by StockTitan Argus on the day of publication.
Key Figures
Market Reality Check
Peers on Argus
B gained 1.39% while gold peers were mixed: WPM +0.45%, FNV +1.51%, AEM +1.06%, AU -0.52%, KGC -0.04%. Moves do not show a uniform sector trend.
Historical Context
| Date | Event | Sentiment | Move | Catalyst |
|---|---|---|---|---|
| Jan 07 | Earnings timing | Neutral | -1.0% | Announced date and webcast details for FY and Q4 2025 results. |
| Jan 07 | Strategic partnership | Positive | -1.0% | Hexagon Robotics partnership with Microsoft on humanoid robot development. |
| Dec 15 | Product integration | Positive | +0.6% | Kennametal–Hexagon integration to deliver faster, smarter machining. |
| Dec 12 | Conference participation | Neutral | -0.1% | Cereno Scientific attendance at JPM Week and Biotech Showcase 2026. |
| Dec 11 | Industry recognition | Positive | +3.3% | ETQ named Front Runner in LNS Research EQMS matrix. |
Recent news, including partnerships and industry recognition, has mostly seen price moves that align with the generally positive or neutral tone, with one notable divergence after a strategic partnership announcement.
Over the past months, news linked to ticker B has covered diverse businesses using the symbol, including earnings timing on February 5, 2026, a strategic robotics partnership with Microsoft on January 7, 2026, and software recognition for ETQ on December 11, 2025. Cereno Scientific-related news on December 12, 2025 highlighted HDAC portfolio progress and Phase I data for CS014. Today’s peer-reviewed CS014 publication and Phase I safety confirmation extend that narrative of advancing HDAC-based cardiopulmonary candidates.
Market Pulse Summary
This announcement highlights peer-reviewed validation of CS014 as a novel HDAC inhibitor with antithrombotic activity while preserving hemostasis, plus favorable Phase I safety data and plans for Phase II in idiopathic pulmonary fibrosis. In recent months, Cereno Scientific has emphasized its HDAC portfolio at conferences and through prior updates. Investors may watch for concrete Phase II trial initiations, additional safety and efficacy readouts, and partnering activity to gauge how this platform matures.
Key Terms
hdac inhibitor medical
nce medical
hemostasis medical
histone deacetylase medical
pharmacology medical
tpa mrna medical
valproic acid medical
idiopathic pulmonary fibrosis medical
AI-generated analysis. Not financial advice.
The manuscript, "Novel HDAC inhibitor, CS014, attenuates in vivo thrombosis while maintaining hemostasis," characterizes CS014 as a novel histone deacetylase (HDAC) inhibitor, engineered to improve upon valproic acid (VPA) through reduced hepatotoxicity risk while preserving the mechanistic benefits of HDAC inhibition. The work shows that CS014 maintains efficacious HDAC inhibitory activity, increases tPA mRNA expression and produces strong antithrombotic effects in small artery, large artery and large vein models. Notably, CS014 achieves these effects while preserving normal coagulation and bleeding time, and it produces substantially lower levels of the hepatotoxic 4-ene metabolite compared with VPA in, in vitro and in vivo systems. Together, these findings support CS014 as a differentiated and potentially safer HDAC inhibitor with broad therapeutic potential in thrombotic and fibrosis-driven diseases.
"CS014 was designed to retain the epigenetic properties of HDAC inhibition of VPA while aiming to improve its safety and metabolic profile," said Dr. Rahul Agrawal, CMO & Head of R&D at Cereno Scientific. "This publication describes how the data supports the rationale behind that design, clearly demonstrating potent antithrombotic activity without increased bleeding risk. These data further validate the HDAC inhibitor mechanism supporting CS014 as a promising candidate for the treatment of cardiovascular and pulmonary diseases where thrombosis, vascular remodeling, and fibrosis play key roles."
"This publication represents a strategically important milestone for Cereno Scientific," said Sten R. Sörensen, CEO at Cereno Scientific. "It is the first formal scientific introduction of our NCE CS014 to the global community and further validates the strength of our HDAC inhibitor platform. Published data is a critical component of partner discussions, regulatory interactions, providing credible scientific status. With the growing external recognition of our science, we are well positioned to advance CS014 as a key value driver in our pipeline."
CS014 recently delivered positive Phase I results confirming that CS014 has a favorable safety profile and is well tolerated at and above exposure levels that, based on non-clinical data, are predicted to support maximal effects on the reversal of pulmonary vascular remodeling and fibrosis. These findings support further clinical evaluation in patients and indicate a broader potential of CS014 in patients with severe cardiovascular and pulmonary diseases involving pulmonary vascular remodeling and fibrosis. Cereno Scientific continues preparations for Phase II development with an initial focus on idiopathic pulmonary fibrosis (IPF).
Access to the manuscript: Stanger, Livia et al. (2025) Novel histone deacetylase inhibitor, CS014, attenuates in vivo thrombosis while maintaining hemostasis. Journal of Thrombosis and Haemostasis. https://doi.org/10.1016/j.jtha.2025.11.011.
For further information, please contact:
Tove Bergenholt, Head of IR & Communications
Email: tove.bergenholt@cerenoscientific.com
Phone: +46 73- 236 62 46
About CS014
CS014 is being developed as a next-generation HDAC inhibitor and novel chemical entity designed to modulate epigenetic pathways that target the root cause of cardiovascular and pulmonary diseases. Non-clinical studies have demonstrated potent effects on pathways involved in vascular remodeling and fibrosis, which are key drivers of disease progression in several cardiovascular and pulmonary conditions and suggests disease-modifying potential. The recently completed Phase I study confirmed that CS014 has a favorable safety profile and is well tolerated at and above exposure levels that, based on non-clinical data, are predicted to support maximal effects on the reversal of pulmonary vascular remodeling and fibrosis. These findings support advancement of CS014 into Phase II clinical development with an initial focus on idiopathic pulmonary fibrosis (IPF). Cereno Scientific is advancing CS014 as a potential new treatment for patients with severe, progressive cardiovascular and pulmonary diseases that currently lack effective therapies.
About Cereno Scientific AB
Cereno Scientific is pioneering treatments to enhance and extend life. The company's innovative pipeline offers disease-modifying drug candidates to empower people suffering from rare cardiovascular and pulmonary diseases to live life to the fullest.
Lead candidate CS1 is an HDAC inhibitor that works through epigenetic modulation and represents a novel therapeutic approach by targeting the root mechanisms of the pulmonary arterial hypertension (PAH). CS1 is a well-tolerated oral therapy with a favorable safety profile that has shown encouraging efficacy signals in a Phase IIa trial in patients with PAH, including improvements in right heart function and patient quality of life, consistent with reverse vascular remodeling. An Expanded Access Program enables patients that have completed the Phase IIa trial to gain access to CS1. CS014, a new chemical entity with disease-modifying potential, showed favorable safety and tolerability profile in a Phase I trial. CS014 is a HDAC inhibitor with a multimodal mechanism of action as an epigenetic modulator having the potential to address the underlying pathophysiology of rare cardiovascular and pulmonary diseases with high unmet needs such as idiopathic pulmonary fibrosis (IPF). Cereno Scientific is also pursuing a preclinical program with CS585, an oral, highly potent and selective prostacyclin (IP) receptor agonist that has demonstrated the potential to significantly improve disease mechanisms relevant to cardiovascular diseases. While CS585 has not yet been assigned a specific indication for clinical development, preclinical data indicates that it could potentially be used in indications like thrombosis prevention without increased risk of bleeding.
The Company is headquartered in GoCo Health Innovation City, in
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The following files are available for download:
Press release |
View original content:SOURCE Cereno Scientific
FAQ
What did Cereno Scientific announce about CS014 on January 14, 2026 (B)?
How does CS014 compare to valproic acid (VPA) according to Cereno (B)?
What efficacy and safety findings were reported for CS014 in nonclinical models (B)?
What clinical progress did Cereno report for CS014 and next steps (B)?
Where was the CS014 manuscript published and how can I access it (B)?
