This “Myocardial Infarction - Pipeline Insight, 2024” report provides comprehensive insights about 48+ companies and 50+ pipeline drugs in Myocardial Infarction pipeline landscape. It covers the pipeline drug profiles, including clinical and nonclinical stage products. It also covers the therapeutics assessment by product type, stage, route of administration, and molecule type. It further highlights the inactive pipeline products in this space.
From a pathologic perspective, MI is defined as cardiomyocyte death caused by an ischemic insult. Application of this definition in the clinical context is challenging because the diagnosis of MI is dependent on the sensitivity and specificity of the clinical criteria, electrocardiographic findings, imaging studies, and biomarkers used to detect the death of cardiomyocytes. In recent years, the development of highly sensitive biomarkers (such as cardiac troponins) has significantly enhanced the clinician’s ability to see cardiomyocyte death. It should be emphasized that, although sudden elevations in circulating troponin levels reflect myocardial injury, they are not specific markers of ischemic cardiomyocyte death but in some cases may reflect increased cell wall permeability or release of proteolytic troponin degradation products. Besides, the slow average turnover of cardiomyocytes may be responsible for modest persistent elevations of troponin levels in specific normal individuals. Moreover, histological evidence of cardiomyocyte death may be present in the absence of ischemia. For example, in animal models, cryoinjury results in sudden and extensive cardiomyocyte necrosis caused by ischemia. In human patients, chronic heart failure, renal failure, myocarditis, and other conditions may cause the nonischemic death of a significant number of cardiomyocytes.
MI is a consequence of an imbalance between oxygen supply and demand. As plaques accumulate gradually, a severe atherosclerotic disease resulting in ≥75% luminal narrowing does not cause a reduction in blood flow at rest. However, when myocardial demand is increased (due to exercise, tachyarrhythmia, etc.), the flow restriction precludes an increase in oxygen supply, resulting in ischemia and causing angina pectoris. In the vast majority of cases, MI results from coronary atherosclerotic disease complicated by superimposed thrombosis. Plaque rupture is the most frequent cause of thrombosis, as a gap in the fibrous cap of a vulnerable plaque exposes the necrotic core to the blood and elicits a potent thrombogenic response. Although most patients with MI have significant obstructive coronary disease, occasionally plaque rupture and ulceration can occur in the absence of an angiographically obstructive lesion. In addition, a wide range of rare conditions may result in occlusion or severe narrowing of the coronary vessels causing nonatherosclerotic MI. Coronary embolism due to endocarditis, prosthetic valve thrombosis, coronary artery dissection, and arthritis due to autoimmune or infectious causes are well-recognized causes of MI in the absence of atherosclerotic disease. Pathophysiologic conditions that contribute to the imbalance between supply and demand participate in the pathogenesis of MI often. Coronary vasospasm and endothelial dysfunction may significantly reduce myocardial blood supply in the presence or absence of an obstructive lesion; severe anemia may reduce oxygen delivery to the myocardium. On the other hand, conditions associated with increased myocardial oxygen demand (such as thyrotoxicosis, aortic stenosis, or cocaine abuse) may precipitate infarction despite a relatively modest reduction in supply.
Diagnosis is based on typical clinical features, ECG findings, and elevation of cardiac biomarkers. Definitive diagnosis requires cardiac catheterization, which serves both diagnostic and therapeutic purposes. All patients suspected of having ACS should be considered for emergency revascularization; additional aspects of treatment include anticoagulation, antiplatelet therapy, statin therapy, and other adjunctive measures. Secondary prevention consists of dual antiplatelet therapy, the initiation of beta-blocker and/or ACE inhibitors, statin therapy, and addressing any modifiable risk factors.
"Myocardial Infarction - Pipeline Insight, 2024" report outlays comprehensive insights of present scenario and growth prospects across the indication. A detailed picture of the Myocardial Infarction pipeline landscape is provided which includes the disease overview and Myocardial Infarction treatment guidelines. The assessment part of the report embraces, in depth Myocardial Infarction commercial assessment and clinical assessment of the pipeline products under development. In the report, detailed description of the drug is given which includes mechanism of action of the drug, clinical studies, NDA approvals (if any), and product development activities comprising the technology, Myocardial Infarction collaborations, licensing, mergers and acquisition, funding, designations and other product related details.
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Geography Covered
- Global coverage
Myocardial Infarction: Understanding
Myocardial Infarction: Overview
Myocardial infarction (MI) refers to ischemic necrosis of myocardial tissue. The most common underlying cause is coronary artery disease. Type 1 MI occurs when an unstable plaque ruptures, leading to the occlusion of a coronary artery. Type 2 MI occurs when there is a mismatch between oxygen supply and demand (e.g., systemic hypotension, vasospasm). MI manifests clinically with acute coronary syndrome (ACS), a potentially lethal condition.From a pathologic perspective, MI is defined as cardiomyocyte death caused by an ischemic insult. Application of this definition in the clinical context is challenging because the diagnosis of MI is dependent on the sensitivity and specificity of the clinical criteria, electrocardiographic findings, imaging studies, and biomarkers used to detect the death of cardiomyocytes. In recent years, the development of highly sensitive biomarkers (such as cardiac troponins) has significantly enhanced the clinician’s ability to see cardiomyocyte death. It should be emphasized that, although sudden elevations in circulating troponin levels reflect myocardial injury, they are not specific markers of ischemic cardiomyocyte death but in some cases may reflect increased cell wall permeability or release of proteolytic troponin degradation products. Besides, the slow average turnover of cardiomyocytes may be responsible for modest persistent elevations of troponin levels in specific normal individuals. Moreover, histological evidence of cardiomyocyte death may be present in the absence of ischemia. For example, in animal models, cryoinjury results in sudden and extensive cardiomyocyte necrosis caused by ischemia. In human patients, chronic heart failure, renal failure, myocarditis, and other conditions may cause the nonischemic death of a significant number of cardiomyocytes.
MI is a consequence of an imbalance between oxygen supply and demand. As plaques accumulate gradually, a severe atherosclerotic disease resulting in ≥75% luminal narrowing does not cause a reduction in blood flow at rest. However, when myocardial demand is increased (due to exercise, tachyarrhythmia, etc.), the flow restriction precludes an increase in oxygen supply, resulting in ischemia and causing angina pectoris. In the vast majority of cases, MI results from coronary atherosclerotic disease complicated by superimposed thrombosis. Plaque rupture is the most frequent cause of thrombosis, as a gap in the fibrous cap of a vulnerable plaque exposes the necrotic core to the blood and elicits a potent thrombogenic response. Although most patients with MI have significant obstructive coronary disease, occasionally plaque rupture and ulceration can occur in the absence of an angiographically obstructive lesion. In addition, a wide range of rare conditions may result in occlusion or severe narrowing of the coronary vessels causing nonatherosclerotic MI. Coronary embolism due to endocarditis, prosthetic valve thrombosis, coronary artery dissection, and arthritis due to autoimmune or infectious causes are well-recognized causes of MI in the absence of atherosclerotic disease. Pathophysiologic conditions that contribute to the imbalance between supply and demand participate in the pathogenesis of MI often. Coronary vasospasm and endothelial dysfunction may significantly reduce myocardial blood supply in the presence or absence of an obstructive lesion; severe anemia may reduce oxygen delivery to the myocardium. On the other hand, conditions associated with increased myocardial oxygen demand (such as thyrotoxicosis, aortic stenosis, or cocaine abuse) may precipitate infarction despite a relatively modest reduction in supply.
Diagnosis is based on typical clinical features, ECG findings, and elevation of cardiac biomarkers. Definitive diagnosis requires cardiac catheterization, which serves both diagnostic and therapeutic purposes. All patients suspected of having ACS should be considered for emergency revascularization; additional aspects of treatment include anticoagulation, antiplatelet therapy, statin therapy, and other adjunctive measures. Secondary prevention consists of dual antiplatelet therapy, the initiation of beta-blocker and/or ACE inhibitors, statin therapy, and addressing any modifiable risk factors.
"Myocardial Infarction - Pipeline Insight, 2024" report outlays comprehensive insights of present scenario and growth prospects across the indication. A detailed picture of the Myocardial Infarction pipeline landscape is provided which includes the disease overview and Myocardial Infarction treatment guidelines. The assessment part of the report embraces, in depth Myocardial Infarction commercial assessment and clinical assessment of the pipeline products under development. In the report, detailed description of the drug is given which includes mechanism of action of the drug, clinical studies, NDA approvals (if any), and product development activities comprising the technology, Myocardial Infarction collaborations, licensing, mergers and acquisition, funding, designations and other product related details.
Report Highlights
The companies and academics are working to assess challenges and seek opportunities that could influence Myocardial Infarction R&D. The therapies under development are focused on novel approaches to treat/improve Myocardial Infarction.Myocardial Infarction Emerging Drugs Chapters
This segment of the Myocardial Infarction report encloses its detailed analysis of various drugs in different stages of clinical development, including phase III, II/III, II, I, preclinical and discovery. It also helps to understand clinical trial details, expressive pharmacological action, agreements and collaborations, and the latest news and press releases.Myocardial Infarction Emerging Drugs
FARXIGA: AstraZeneca
FARXIGA (known as FORXIGA outside the US) (dapagliflozin) is a first-in-class, oral, once-daily SGLT2 inhibitor. Research has shown FARXIGA’s efficacy in preventing and delaying cardiorenal disease while protecting the organs - important findings given the underlying links between the heart, kidneys, and pancreas. The drug is currently being evaluated under Phase III clinical trial for the treatment of patients with Myocardial Infarction.KAND567: Kancera
The drug candidate KAND567, developed by Kancera, inhibits the chemokine CXCL13 and protects the heart and blood vessels from injuries associated with AMI. The drug is currently being evaluated under Phase II clinical trial for the treatment of patients with Myocardial Infarction.TWB201: Taiwan Bio Therapeutics
TWB201, is an investigational non-modified mesenchymal stem cell therapy developed by Taiwan Bio Therapeutics. The drug is currently being evaluated under Phase I clinical trial for the treatment of patients with Myocardial Infarction.Myocardial Infarction: Therapeutic Assessment
This segment of the report provides insights about the different Myocardial Infarction drugs segregated based on following parameters that define the scope of the report, such as:Major Players in Myocardial Infarction
There are approx. 48+ key companies which are developing the therapies for Myocardial Infarction. The companies which have their Myocardial Infarction drug candidates in the most advanced stage, i.e. Phase III include, AstraZeneca.Phases
This report covers around 50+ products under different phases of clinical development like
- Late stage products (Phase III)
- Mid-stage products (Phase II)
- Early-stage product (Phase I) along with the details of
- Pre-clinical and Discovery stage candidates
- Discontinued & Inactive candidates
Route of Administration
Myocardial Infarction pipeline report provides the therapeutic assessment of the pipeline drugs by the Route of Administration. Products have been categorized under various ROAs such as- Intravenous
- Subcutaneous
- Oral
- Intramuscular
- Molecule Type
Products have been categorized under various Molecule types such as
- Monoclonal antibody
- Small molecule
- Peptide
- Product Type
Myocardial Infarction: Pipeline Development Activities
The report provides insights into different therapeutic candidates in phase II, I, preclinical and discovery stage. It also analyses Myocardial Infarction therapeutic drugs key players involved in developing key drugs.Pipeline Development Activities
The report covers the detailed information of collaborations, acquisition and merger, licensing along with a thorough therapeutic assessment of emerging Myocardial Infarction drugs.Myocardial Infarction Report Insights
- Myocardial Infarction Pipeline Analysis
- Therapeutic Assessment
- Unmet Needs
- Impact of Drugs
Myocardial Infarction Report Assessment
- Pipeline Product Profiles
- Therapeutic Assessment
- Pipeline Assessment
- Inactive drugs assessment
- Unmet Needs
Key Questions
Current Treatment Scenario and Emerging Therapies:
- How many companies are developing Myocardial Infarction drugs?
- How many Myocardial Infarction drugs are developed by each company?
- How many emerging drugs are in mid-stage, and late-stage of development for the treatment of Myocardial Infarction?
- What are the key collaborations (Industry-Industry, Industry-Academia), Mergers and acquisitions, licensing activities related to the Myocardial Infarction therapeutics?
- What are the recent trends, drug types and novel technologies developed to overcome the limitation of existing therapies?
- What are the clinical studies going on for Myocardial Infarction and their status?
- What are the key designations that have been granted to the emerging drugs?
Key Players
- AstraZeneca
- Kancera
- Taiwan Bio Therapeutics
- Translational Sciences
- RION
- Mesoblast
- Faraday Pharmaceuticals
- Idorsia Pharmaceuticals
- Celecor Therapeutics
- ResoTher Pharma
- BioCardia
- TRPHARM
Key Products
- FARXIGA
- KAND567
- TWB201
- TS 23
- Purified exosome product
- MPC-25-IC
- FDY-5301
- Selatogrel
- Zalunfiban
- RTP 026
- CardiALLO cell therapy
- Goflikicept
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Table of Contents
IntroductionExecutive SummaryMyocardial Infarction- Analytical PerspectiveMyocardial Infarction Key CompaniesMyocardial Infarction Key ProductsMyocardial Infarction- Unmet NeedsMyocardial Infarction- Market Drivers and BarriersMyocardial Infarction- Future Perspectives and ConclusionMyocardial Infarction Analyst ViewsMyocardial Infarction Key CompaniesAppendix
Myocardial Infarction: Overview
Pipeline Therapeutics
Therapeutic Assessment
Late Stage Products (Phase III)
FARXIGA: AstraZeneca
Mid Stage Products (Phase II)
KAND567: Kancera
Early Stage Products (Phase I)
TWB201: Taiwan Bio Therapeutics
Preclinical and Discovery Stage Products
Drug name: Company name
Inactive Products
List of Tables
Companies Mentioned (Partial List)
A selection of companies mentioned in this report includes, but is not limited to:
- AstraZeneca
- Kancera
- Taiwan Bio Therapeutics
- Translational Sciences
- RION
- Mesoblast
- Faraday Pharmaceuticals
- Idorsia Pharmaceuticals
- Celecor Therapeutics
- ResoTher Pharma
- BioCardia
- TRPHARM