Draft:Cardior Pharmaceuticals: Difference between revisions
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{{AFC comment|1=Too many issues. |
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Revision as of 15:25, 10 January 2024
| Submission declined on 10 January 2024 by Mach61 (talk). This submission provides insufficient context for those unfamiliar with the subject matter. Please see the guide to writing better articles for information on how to better format your submission.
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This draft has not been edited in over six months and qualifies to be deleted per CSD G13. Declined by Mach61 11 months ago. Last edited by Mach61 11 months ago. Reviewer: Inform author.
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| Submission declined on 16 June 2023 by Carpimaps (talk). This submission is not adequately supported by reliable sources. Reliable sources are required so that information can be verified. If you need help with referencing, please see Referencing for beginners and Citing sources. This draft's references do not show that the subject qualifies for a Wikipedia article. In summary, the draft needs multiple published sources that are: Declined by Carpimaps 18 months ago.
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Comment: Too many issues.1. The article seems to stray from its original topic and talks about RNA? Please remove unrelated information.2. The company's website is no way a reliable source for biomedical information. Please look through Wikipedia:Identifying reliable sources (medicine). Carpimaps talk to me! 14:03, 16 June 2023 (UTC)
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| Company type | GmbH |
|---|---|
| Industry | Biotechnology |
| Founded | 2016 in Hanover, Germany |
| Founders | Prof. Dr. Dr. Thomas Thum Dr. Claudia Ulbrich Dr. Sandor Batkai |
| Headquarters | Hollerithallee 20, 30419 Hannover , Germany |
Key people | Dr. Claudia Ulbrich (CEO) Prof. Dr. Dr. Thomas Thum (CMO/CSO) Axel-Sven Malkomes (CFO) |
Number of employees | 27 (2023) |
| Website | cardior |
Cardior Pharmaceuticals GmbH is a clinical-stage biopharmaceutical company based in Hanover Germany founded in 2016. The company is developing curative and preventive heart failure therapeutics based on non-coding RNAs (ncRNAs).[1]
Scientific approach
Cardior’s approach is based on the latest research in non-coding RNAs[2] biology and addresses the root causes of heart failure (HF) development. Non-coding RNAs (ncRNAs) are important regulators for many cellular processes, particularly in pathological condition or during disease. In heart disease or following cardiac stress such as myocardial infarction (MI), the human heart undergoes a process termed cardiac remodeling. This is initially an adaptive response, but it soon leads to pathological cardiac hypertrophy, fibrosis altering the biomechanical properties of the heart, and finally to impairment of contractility function so the heart is unable to effectively pump blood through the body and deliver enough oxygen and nutrients to the organs.[3] Currently available therapeutic solutions deal with the consequences of heart failure, alleviate the symptoms but do not halt its development.
MicroRNA-132 (miR-132), present in cytoplasm of cardiac muscle cells, was identified by Hannover Medical School (MHH) as an important indicator of cardiac stress and the main trigger of cardiac remodeling.[4] An increase of miR-132 in cardiac tissue drives abnormal expression of genes that are crucially involved in cardiac function and derail cellular signaling leading to cardiac remodeling and heart failure.
CDR132L - Cardior’s lead candidate - is designed to address the root cause of pathological remodeling of the heart following MI and thereby halt and reverse the detrimental signaling cascade and restore normal function of the heart.[5] CDR132L blocks abnormal levels of miR-132 thus triggering a concerted therapeutic effect against key hallmarks of heart disease by normalization of derailed gene expression signatures. These include expression of genes regulating cardiac hypertrophy, fibrosis, impaired contractility, and reduced vascularization.
Initially evaluated in mice with pressure-overload induced heart failure and in miR-132 transgenic HF mouse models, CDR132L treatment reduced functional miR-132 level and reversed cardiac dilatation along with an improvement of cardiac function. The safety and therapeutic efficacy of CDR132L was further assessed in numerous large animal models.[6][7][8]
Clinical study
The first-in-human Phase 1b clinical study confirmed CDR132L to be safe and well-tolerated having demonstrated first beneficial cardiac signs in heart failure patients[9](NCT04045405)[10] CDR132L is currently being investigated in the company’s Phase 2 HF-REVERT trial. [11] HF-REVERT is a multicenter, randomized, parallel 3-arm, placebo-controlled study to assess the efficacy and safety of CDR132L in 280 patients with reduced LVEF after myocardial infarction. The study is being conducted at over 70 clinical study centers across Europe.
CardiorHealth miR-132 PCR kit
Cardior has developed a PCR kit to measure the levels of microRNA-132 (miR-132) circulating in the blood of the patients receiving the company’s lead candidate CDR132L, an oligonucleotide-based miR-132 inhibitor. The marking for CardiorHealth miR-132 PCR kit was received in September 2022. CE Marking is an acronym for the French “Conformité Européenne” certifying that a product has met EU health, safety, and environmental requirements, which ensure consumer safety.
Financing
BioMedPartners, Bristol Myers Squibb, Coparion, EQT, Fund+, Hadean Ventures, INKEF Capital, High-Tech Gründefunds, Sunstone.
Patents
Cardior holds an IP portfolio of over 150 patents and applications in 35 countries exclusively licensed to or owned by the Company.
Timeline
- 2016 - Cardior Pharmaceuticals GmbH founded in Hanover, Germany
- 2017 - Lead compound selection
- 2020 - Phase 1b Clinical Study completed
- 2022 - Start of HF-REVERT Phase 2 Study in heart failure patients
References
- ^ Sheridan, Cormac (2023-04-04). "Genetic medicines aim straight for the heart". Nature Biotechnology. 41 (4): 435–437. doi:10.1038/s41587-023-01745-4. PMID 37016163. S2CID 257952774.
- ^ Nemeth, Kinga; Bayraktar, Recep; Ferracin, Manuela; Calin, George A. (2023-11-15). "Non-coding RNAs in disease: from mechanisms to therapeutics". Nature Reviews Genetics: 1–22. doi:10.1038/s41576-023-00662-1. ISSN 1471-0064.
- ^ Bauersachs, Johann; Butler, Javed; Sandner, Peter (9 June 2017). Heart Failure. Springer. ISBN 978-3-319-59659-4.
- ^ Ucar, A; Gupta, SK; et al. (2012). "The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy". Nat. Commun. 3 (3): 1078. Bibcode:2012NatCo...3.1078U. doi:10.1038/ncomms2090. PMC 3657998. PMID 23011132.
- ^ Viereck, Janika; Thum, Thomas. "Development of a Mechanism-Based Next-Generation Therapeutic for Heart Failure Derived From the Dark Genome". JACC: Basic to Translational Science. 8 (12): 1595–1598. doi:10.1016/j.jacbts.2023.09.006.
- ^ Foinquinos, A.; Batkai, S.; Genschel, C.; et, al (2020). "Preclinical development of a miR-132 inhibitor for heart failure treatment". Nat. Commun. 11 (1): 633. Bibcode:2020NatCo..11..633F. doi:10.1038/s41467-020-14349-2. PMC 6994493. PMID 32005803.
- ^ Batkai, S.; Genschel, C.; Viereck, J.; et, al. (2021). "CDR132L improves systolic and diastolic function in a large animal model of chronic heart failure". Eur. Heart J. 42 (2): 192–201. doi:10.1093/eurheartj/ehaa791. PMC 7813625. PMID 33089304.
- ^ Hinkel, R.; Batkai, S; Bähr, A.; et, al. (2021). "AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction". J Am Coll Cardiol. 77 (23): 2923–35. doi:10.1016/j.jacc.2021.04.028.
- ^ Täubel, J; Hauke, W; Rump, S; et, al (2021). "Novel antisense therapy targeting microRNA-132 in patients with heart failure: Results of a first-in-human Phase 1b randomized, double-blind, placebo-controlled study". Eur Heart J. 42 (2): 178–88. doi:10.1093/eurheartj/ehaa898. PMID 33245749.
- ^ "NCT04045405". clinical.trials.gov. Retrieved 2023-01-09.
- ^ "NCT05350969". clinical.trials.gov. Retrieved 2023-01-09.
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