All Clinical Trials for angiotensin ii acetate

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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NCT00364000 ↗	Arterial Stiffness and Calcifications in Haemodialysis Patients on Sevelamer or Calcium Acetate	Withdrawn	Romanian Society of Nephrology	N/A	2012-01-01	End-stage renal disease (ESRD) is a state of increased arterial stiffness of extensive vessel calcifications,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.
NCT01135615 ↗	Sevelamer, FGF-23 and Endothelial Dysfunction in Chronic Kidney Disease (CKD)	Completed	Gulhane School of Medicine	Phase 4	2008-01-01	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 FGF23 levels concentrations and ED seen in CKD patients. The researchers investigated the relationship between plasma FGF23 levels and the forearm blood flow response to ischemia in the forearm in a sizable series of incident stage 3-4 CKD patients.
>Trial ID	>Title	>Status	>Sponsor	>Phase	>Start Date	>Summary

Condition Name for angiotensin ii acetate
Alcoholic Liver Cirrhosis	1
Ascites	1
Cough	1
Haemodialyzed Patients	1
[disabled in preview]	1
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Condition MeSH for angiotensin ii acetate
Coronary Disease	1
Liver Cirrhosis	1
Coronary Artery Disease	1
Fibrosis	1
[disabled in preview]	1
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Trials by Country for angiotensin ii acetate
United States	5
Romania	1
Egypt	1
Denmark	1
Turkey	1
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Trials by US State for angiotensin ii acetate
North Carolina	1
New York	1
Missouri	1
Indiana	1
Colorado	1
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Clinical Trial Phase for angiotensin ii acetate
Phase 4	3
Phase 2	1
N/A	2
[disabled in preview]	0
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Clinical Trial Status for angiotensin ii acetate
Completed	4
Unknown status	1
Withdrawn	1
[disabled in preview]	0
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Sponsor Name for angiotensin ii acetate
Gulhane School of Medicine	2
National Heart, Lung, and Blood Institute (NHLBI)	1
Johns Hopkins University	1
[disabled in preview]	4
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Sponsor Type for angiotensin ii acetate
Other	10
NIH	1
[disabled in preview]	0
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Last updated: May 3, 2026

What is angiotensin II acetate and where is it used clinically?

Angiotensin II acetate is a synthetic form of angiotensin II administered to increase blood pressure through the angiotensin II receptor pathway (primarily AT1), producing vasoconstriction and supporting renal perfusion. Clinically, the product class has been developed for refractory vasodilatory shock after standard therapies, with the most established market positioning centered on catecholamine-resistant or catecholamine-dependent hypotension in intensive care settings.

In commercial use, the drug’s regulatory footprint and clinical evidence base are tied to specific shock phenotypes and guideline-consistent vasopressor escalation pathways. The product name most directly associated with angiotensin II acetate is Giapreza (angiotensin II) (available in multiple jurisdictions; dosing typically targets rapid reversal of hypotension in refractory shock).

What does the clinical evidence landscape look like (core trials and endpoints)?

Clinical development has been structured around hemodynamic endpoints (blood pressure response) and safety outcomes relevant to ICU care. The most cited pivotal dataset supporting approval has focused on:

Durable blood pressure response (commonly systolic blood pressure or MAP response criteria within a defined assessment window)
Time to achieve hemodynamic stability
Vasopressor dose reduction and ability to wean from other pressors
Safety in shock populations, with special attention to ischemic events and renal complications

These trials informed labeling requirements that typically restrict use to patients with hypotension despite fluids and catecholamine vasopressors. FDA review documentation and pivotal study reporting define the regulatory threshold for approval. (See pivotal trial and regulatory review materials in sources [1] and [2].)

What is the current clinical trials status?

As of the latest accessible registry and publication record tied to angiotensin II acetate, the clinical trials landscape is dominated by post-approval studies and safety/real-world evaluations rather than new phase 3 confirmatory programs. The most visible trial programs are:

Ongoing or completed post-marketing observational work focusing on:
- ICU mortality and length of stay
- ischemic adverse events (arterial thrombosis, digital ischemia, mesenteric ischemia in severe vasoconstriction contexts)
- renal outcomes, including dialysis initiation
Expanded use evaluations in specific subgroups:
- patients with different baseline severity
- shock-refractory subpopulations where vasopressor responsiveness varies

Trial activity is tracked across public registries, with study status and dates updated over time. A comprehensive trial-level mapping requires direct registry extraction at the time of reporting; the clinically anchored interpretation below aligns with what is consistently reported in approval documentation and follow-on publications. (Sources: FDA clinical review [2]; registry and trial publications indexed in [1] and [3].)

Is there any material new phase 3 signal that changes the risk-benefit profile?

No material new phase 3 signal is established in the public record for angiotensin II acetate that would reset efficacy expectations or materially expand the labeled indication beyond what was supported at approval. The post-approval evidence base is dominated by real-world confirmatory use and safety surveillance. This matters for market projection because it limits near-term label expansion catalysts to observational or subgroup-confirmatory outcomes rather than full-scale efficacy rescoping.

Regulatory and Label Footprint: What approvals constrain the market?

Where is angiotensin II acetate approved and how do labels define usage?

The approval pathway is centered on ICU shock with refractory hypotension. Biopharma market access hinges on:

Eligibility criteria (fluids, catecholamine vasopressor failure)
Dosing windows and infusion control rules
Safety monitoring obligations linked to ischemic events and renal outcomes

FDA labeling and review artifacts constrain use to the shock setting supported by pivotal trials and review methodology. (Sources: FDA label and clinical review package [2].)

What safety outcomes drive clinician prescribing discipline?

Across shock populations, vasoconstrictor agents create predictable risk trade-offs. For angiotensin II acetate, risk management focuses on ischemic events and perfusion-related safety signals. The pivotal review documents the safety evaluation approach and adjudication of clinically meaningful ischemic events. (Source [2].)

This is central to market uptake because payer authorization and hospital protocol adoption typically require:

documented shock refractoriness
contraindication screening
protocolized monitoring for ischemia and organ perfusion

Commercial Market Analysis: How big is the addressable opportunity?

What is the addressable market in refractory vasodilatory shock?

The market is defined by ICU incidence of vasodilatory shock states where catecholamine therapy fails or requires escalation, and where clinical practice supports use of a second-line pressor with a distinct mechanism. The practical addressable population is smaller than global shock incidence because:

many patients respond to escalating catecholamines and vasopressin analog strategies
some hospitals follow protocols that limit use of angiotensin II to specific stewardship pathways
reimbursement and formulary placement influence uptake

Market sizing for angiotensin II acetate therefore models:

ICU shock volume (US plus EU5 plus other developed markets)
percent of patients with catecholamine-resistant or dependent hypotension
adoption curve driven by guideline alignment, formulary access, and physician comfort with ischemic risk

How fast can hospitals adopt angiotensin II acetate?

Adoption is typically limited by:

protocolization requirements for refractory shock
training on monitoring and infusion management
internal safety governance due to ischemic event risk

This drives a slower initial uptake curve that later normalizes as order set inclusion and pharmacy integration increases. Market penetration often rises when:

formularies establish criteria and pre-authorization pathways
intensivist societies and guideline panels cite the evidence base
real-world usage reduces perceived uncertainty

Pricing and reimbursement mechanics: what affects revenue capture?

Revenue capture depends on:

per-vial/per-treatment pricing aligned to infusion duration and dosing
payer policy for coverage of “refractory” shock
hospital contracts that favor “ICU shock pathway” products

Because the drug is administered in acute ICU episodes, procurement is driven by pharmacy and therapeutics committees rather than chronic care formularies. The most material revenue swings are driven by:

guideline reinforcement
payer edits on eligibility criteria
hospital utilization protocols

Market Projection: Revenue outlook and utilization trajectory

What are the main drivers of growth?

For angiotensin II acetate, growth typically comes from four levers:

ICU volume growth and shock case mix shifts
Higher adoption in catecholamine-refractory segments as clinicians gain experience
Formulary wins and contract expansions that reduce friction at the point of care
Broader comfort in safety monitoring lowering hesitation among stewardship committees

What are the main headwinds?

Safety and ischemic risk perceptions that can restrict prescribing to strict protocols
Competition from other second-line vasopressors and combination regimens
Payer restrictions tied to “refractory” definitions
Limited label expansion catalysts without new randomized efficacy evidence

What is the likely 3-year revenue trajectory profile?

Given the evidence base focus on refractory shock and the absence of new phase 3 efficacy redefinition, the most defensible market shape is:

near-term growth driven by adoption and contracting
mid-term growth constrained by safety protocol strictness and reimbursement editing
incremental expansions only if guideline and real-world safety data translate into broader eligibility

In business terms: the slope is set less by scientific upside and more by hospital and payer friction removal.

Competitive Landscape: What other products shape positioning?

Angiotensin II acetate competes in a functional class: ICU vasopressor management after inadequate response to standard therapies. Competitive substitution occurs through:

different vasopressor mechanisms in refractory hypotension pathways
locally preferred order sets (institution-specific)
payer-preferred coverage rules

The commercial implication is that angiotensin II uptake tends to rise when it is positioned as a targeted rescue tool that improves hemodynamics without adding excessive protocol complexity.

Key Takeaways

Angiotensin II acetate is clinically positioned for refractory vasodilatory shock in ICU settings where catecholamines and standard escalation strategies fail to restore adequate blood pressure.
The evidence base supporting use is rooted in pivotal efficacy and safety assessment documented in FDA review materials, with endpoints anchored to hemodynamic response and clinically relevant safety monitoring.
Current development activity is mainly post-approval and real-world/safety surveillance, which limits near-term label expansion catalysts tied to new randomized phase 3 efficacy signals.
Market growth is driven by adoption in catheter-resistant shock segments, formulary and contract coverage, and protocol integration, while constrained by ischemic safety perceptions and payer eligibility definitions.

FAQs

1) What patient population is angiotensin II acetate intended for?

Use is directed at patients with hypotension in refractory shock after fluids and catecholamine vasopressor therapy, consistent with label-supported eligibility and pivotal trial design. [2]

2) What efficacy endpoints matter most in the regulatory evidence?

Regulatory evaluation centers on hemodynamic response durability and related clinical management outcomes used in the pivotal trial assessment framework. [2]

3) What safety concerns most affect hospital adoption?

Clinicians and stewardship committees focus on ischemic and perfusion-related adverse events and organ outcomes in critically ill patients, which drives protocol strictness. [2]

4) Will the next growth phase likely come from new indications?

The public record reflects post-approval evidence generation more than new phase 3 redefinition, so near-term growth is more likely driven by uptake and contracting than major label expansion. [1], [2]

5) How do payers typically control access?

Payers commonly apply criteria tied to refractory definitions, ICU eligibility, and failure of standard therapies, which makes protocolization and documentation key to reimbursement. [2], [3]

References

[1] ClinicalTrials.gov. Angiotensin II studies. https://clinicaltrials.gov/ (accessed 2026-05-03).
[2] U.S. Food and Drug Administration. Clinical Review(s) and Labeling for GIAPREZA (angiotensin II). https://www.accessdata.fda.gov/ (accessed 2026-05-03).
[3] PubMed. Angiotensin II acetate (Giapreza) clinical trial publications indexed. https://pubmed.ncbi.nlm.nih.gov/ (accessed 2026-05-03).

CLINICAL TRIALS PROFILE FOR ANGIOTENSIN II ACETATE