CLINICAL TRIALS PROFILE FOR ANGIOTENSIN II ACETATE

All Clinical Trials for Angiotensin Ii Acetate

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00239096 ↗	Prevention of Decompensation in Liver Cirrhosis	Unknown status	Else Poulsen Mindelegat	Phase 4	2005-09-01	The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic.
NCT00239096 ↗	Prevention of Decompensation in Liver Cirrhosis	Unknown status	Lundbeck Foundation	Phase 4	2005-09-01	The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic.
NCT00239096 ↗	Prevention of Decompensation in Liver Cirrhosis	Unknown status	University of Southern Denmark	Phase 4	2005-09-01	The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic.
NCT00239096 ↗	Prevention of Decompensation in Liver Cirrhosis	Unknown status	Odense University Hospital	Phase 4	2005-09-01	The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic.
NCT00364000 ↗	Arterial Stiffness and Calcifications in Haemodialysis Patients on Sevelamer or Calcium Acetate	Withdrawn	Romanian Society of Nephrology	N/A	2012-01-01	End-stage renal disease (ESRD) is a state of increased arterial stiffness of extensive vessel calcifications, compared with the non-renal population. Both arterial stiffness and arterial calcifications are potent predictors of all-cause and cardiovascular mortality in ESRD patients. Several studies have documented the direct relationship between the extent and severity of arterial/coronary calcifications and outcome in dialysis patients. The relationship is strong no matter if arterial calcifications were quantified by electron-beam computed tomography or a radiological calcification score. Calcifications are early and progressive events in these patients. PWV is strongly related to the degree of sonographic determined arterial calcifications and EBCT-derived coronary artery calcium score in chronic kidney disease patients. Calcium-based phosphate binders are associated with progressive coronary artery and aortic calcification, especially when mineral metabolism is not well controlled. According to recent studies, sevelamer hydrochloride is a potent non-calcium-containing phosphate binder, well tolerated in ESRD. Compared with calcium-based phosphate binders, sevelamer is less likely to cause hypercalcemia, low levels of PTH, and progressive coronary and aortic calcification in hemodialysis patients. Moreover, sevelamer has a favorable effect on the lipid profile. Less is known about the relationship between sevelamer treatment and progression of arterial stiffness. To date, there is one single study examining the influence of sevelamer (versus calcium carbonate) on the evolution of arterial stiffness in a very small number (N=15) of haemodialysis patients. These study used the same patients as historical controls, thus being methodologically rather weak. Moreover, the follow-up was quite short - 6 month. The aim of the trial is to to quantify, in a randomized opened-labeled controlled trial the effect of sevelamer hydrochloride on the evolution of arterial stiffness parameters (pulse wave velocity and the augmentation index) in chronic haemodialysis patients and to correlate these parameters with arterial calcification assessed by a previous described radiological score of arterial calcification and echocardiographic parameters (left ventricular hypertrophy, LV dilatation, systolic and diastolic dysfunction).
NCT00486772 ↗	Sevelamer, Fetuin-A and Endothelial Dysfunction in CKD	Completed	Gulhane School of Medicine	Phase 4	1969-12-31	Vascular calcification and endothelial dysfunction (ED) contribute to the development of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). Sevelamer, a non-calcium based phosphate binder, has been shown to attenuate cardiovascular calcification in CKD patients while the exact mechanism has not been clarified. This study was designed to investigate the effect of short-term sevelamer treatment on both serum fetuin-A concentrations and ED seen in CKD patients.

Clinical Trial Conditions for Angiotensin Ii Acetate

Condition Name

Condition Name for Angiotensin Ii Acetate
Intervention	Trials
We Investigated the Relationship Between Plasma FGF23 Levels and Endothelial Dysfunction in a Sizable Series of Incident Stage 3-4 CKD Patients.	1
Alcoholic Liver Cirrhosis	1
Ascites	1
Cough	1

Condition MeSH

Condition MeSH for Angiotensin Ii Acetate
Intervention	Trials
Fibrosis	1
Cough	1
Ascites	1
Vascular Diseases	1

Clinical Trial Locations for Angiotensin Ii Acetate

Trials by Country

Trials by Country for Angiotensin Ii Acetate
Location	Trials
United States	5
Denmark	1
Turkey	1
Romania	1
Egypt	1

Trials by US State

Trials by US State for Angiotensin Ii Acetate
Location	Trials
North Carolina	1
New York	1
Missouri	1
Indiana	1
Colorado	1

Clinical Trial Progress for Angiotensin Ii Acetate

Clinical Trial Phase

Clinical Trial Phase for Angiotensin Ii Acetate
Clinical Trial Phase	Trials
Phase 4	3
Phase 2	1
N/A	2

Clinical Trial Status

Clinical Trial Status for Angiotensin Ii Acetate
Clinical Trial Phase	Trials
Completed	4
Unknown status	1
Withdrawn	1

Clinical Trial Sponsors for Angiotensin Ii Acetate

Sponsor Name

Sponsor Name for Angiotensin Ii Acetate
Sponsor	Trials
Gulhane School of Medicine	2
Kasr El Aini Hospital	1
Else Poulsen Mindelegat	1

Sponsor Type

Sponsor Type for Angiotensin Ii Acetate
Sponsor	Trials
Other	10
NIH	1

Angiotensin II Acetate: Clinical Trials, Market Analysis, and Projections

Introduction

Angiotensin II acetate, a synthetic peptide identical to human angiotensin II, has been gaining significant attention in the medical field due to its role in managing severe hypotension, particularly in cases of septic or other distributive shock. Here, we will delve into the current state of clinical trials, market analysis, and future projections for this drug.

Clinical Trials Update

ATHOS-3 Clinical Trial

One of the pivotal clinical trials for angiotensin II acetate is the ATHOS-3 trial. This study demonstrated the efficacy of angiotensin II in increasing blood pressure in adults with septic or other distributive shock. Key findings include:

• Efficacy: The trial showed that angiotensin II significantly increased mean arterial pressure (MAP) compared to the placebo group. The median time to reach the target MAP was approximately 5 minutes[3][5].
• Safety: While angiotensin II was effective, it also showed a higher incidence of arterial and venous thrombotic and thromboembolic events, including deep venous thromboses. Other adverse effects included thrombocytopenia, tachycardia, and fungal infections[3][5].

Ongoing and Future Trials

Several clinical trials are ongoing or planned to further evaluate the safety and efficacy of angiotensin II acetate. These trials aim to address various aspects, such as optimal dosing regimens, long-term outcomes, and potential interactions with other medications.

Mechanism of Action

Angiotensin II acetate works by binding to the angiotensin II receptor type 1 (AT1R), leading to strong vasoconstrictive effects. This mechanism is crucial for increasing blood pressure in patients with severe hypotension.

• Pharmacodynamics: Angiotensin II is rapidly metabolized by aminopeptidases A and M into angiotensin III and angiotensin IV, respectively. It has a plasma half-life of less than one minute and reaches steady state within 5 minutes[3][5].

Market Analysis

Current Market Status

Angiotensin II acetate was first approved by the US FDA on December 21, 2017, under the brand name Giapreza (LJPC-501)[1][5].

Market Size and Growth

The market for vasoconstrictors, including angiotensin II acetate, is part of the broader cardiovascular drug market. While specific market size data for angiotensin II acetate is not readily available, the overall market for cardiovascular drugs is significant and growing.

• Cardiovascular Drug Market: The global angiotensin converting enzymes (ACE) inhibitors market, which is closely related, is projected to reach $11,831.7 million by 2030, growing at a CAGR of 5.6% from 2023[2].

Competitive Landscape

The cardiovascular drug market is highly competitive, with several key players focusing on strategic collaborations, product innovations, and geographical expansion. Angiotensin II acetate, being a niche product, faces competition from other vasoconstrictors and vasopressors but has a unique position due to its specific indication and mechanism of action.

Market Projections

Future Growth

The demand for effective treatments for septic and distributive shock is expected to drive the growth of angiotensin II acetate. Here are some key projections:

• Increasing Prevalence: The escalating prevalence of sepsis and other critical care conditions will increase the demand for angiotensin II acetate.
• Advancements in Drug Formulations: Ongoing research and development aimed at enhancing the efficacy and safety profiles of angiotensin II acetate will further propel market growth.
• Regulatory Approvals: Potential approvals in additional regions and for new indications could expand the market reach of angiotensin II acetate[2][3].

Challenges and Opportunities

Challenges

Despite its efficacy, angiotensin II acetate faces several challenges:

• Adverse Effects: The higher incidence of thrombotic and thromboembolic events, as well as other adverse effects, necessitates careful patient monitoring and management[3][5].
• Concomitant Medications: The interaction with ACE inhibitors and angiotensin II blockers (ARBs) requires careful consideration in treatment protocols[3].

Opportunities

There are several opportunities for growth and development:

• Expanding Indications: Potential new indications, such as other forms of shock or critical care conditions, could broaden the market for angiotensin II acetate.
• Combination Therapies: Research into combination therapies involving angiotensin II acetate and other cardiovascular drugs could enhance treatment outcomes and market appeal[2][3].

Key Takeaways

• Clinical Efficacy: Angiotensin II acetate has demonstrated significant efficacy in increasing blood pressure in adults with septic or other distributive shock.
• Market Growth: The market for angiotensin II acetate is expected to grow driven by increasing demand for effective treatments in critical care.
• Challenges: The drug faces challenges related to adverse effects and interactions with other medications.
• Opportunities: There are opportunities for expanding indications and developing combination therapies.

FAQs

What is the primary indication for angiotensin II acetate?

Angiotensin II acetate is indicated for increasing blood pressure in adults with septic or other distributive shock[3].

What are the common adverse effects of angiotensin II acetate?

Common adverse effects include thrombotic and thromboembolic events, thrombocytopenia, tachycardia, and fungal infections[3][5].

How does angiotensin II acetate work?

Angiotensin II acetate works by binding to the angiotensin II receptor type 1 (AT1R), leading to strong vasoconstrictive effects[3].

What is the current market status of angiotensin II acetate?

Angiotensin II acetate was first approved by the US FDA in 2017 under the brand name Giapreza (LJPC-501)[1][5].

What are the future growth prospects for angiotensin II acetate?

The market for angiotensin II acetate is expected to grow due to increasing demand for effective treatments in critical care, advancements in drug formulations, and potential new indications[2][3].

Sources

1. Synapse: Angiotensin II Acetate - Drug Targets, Indications, Patents.
2. Coherent Market Insights: Angiotensin Converting Enzymes (ACE) Inhibitors Market.
3. DrugBank: Angiotensin II: Uses, Interactions, Mechanism of Action.
4. AstraZeneca: Clinical Trials Appendix.
5. FDA: 209360Orig1s000 - accessdata.fda.gov.

Last updated: 2024-12-31