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Angiotensin II

Peptide

Angiotensin II is the endogenous vasoconstrictor peptide now available as a synthetic IV formulation (Giapreza). FDA-approved 2017 for vasodilatory/septic shock refractory to standard vasopressors. A-GRADE evidence from ATHOS-3 (n=321): 70% achieved MAP response vs 23% placebo (P<0.001). Post-hoc analysis: AKI patients on RRT showed 53% vs 30% survival at day 28. SAFETY CONCERN: Increased thromboembolism (13% vs 5%), requires DVT prophylaxis. No mortality benefit in main analysis - approved for hemodynamic response, not survival. PRESCRIPTION ONLY - ICU setting.

Quick Answer

What it is

Angiotensin II is the endogenous vasoconstrictor peptide now available as a synthetic IV formulation (Giapreza). FDA-approved 2017 for vasodilatory/septic shock refractory to standard vasopressors.

Key findings

  • Grade A: Mean Arterial Pressure Response (Septic Shock)
  • Grade A: Vasopressor Dose Reduction (Septic Shock)
  • Grade A: 28-Day Mortality (Septic Shock)

Safety

  • May reduce catecholamine toxicity.
⚠️ Research Notice

This peptide information is for educational and research purposes only. Peptides may not be FDA-approved for human use and may only be legally available for research purposes. Consult qualified healthcare professionals before considering any peptide compounds.

ℹ️ Quick Facts: Angiotensin II

Quick Facts: Angiotensin II

  • Best Evidence:Grade A
  • Conditions Studied:2
  • Research Outcomes:12
  • Grade A Findings:4
  • Grade B Findings:2
  • Key Effect:Septic Shock
A4
B2
C2
D4
2 conditions · 12 outcomes

Detailed Outcomes

|
A
Mean Arterial Pressure Response
ATHOS-3 (n=321): 70% achieved MAP ≥75 mmHg or ≥10 mmHg increase at 3h vs 23% placebo (P<0.001). 45% absolute increase in responders. Effective in catecholamine-resistant shock.
large↑Improves
A
Vasopressor Dose Reduction
ATHOS-3: Significant reduction in background vasopressor requirements. Catecholamine-sparing effect allows reduction of norepinephrine doses. May reduce catecholamine toxicity.
moderate↓Improves
A
28-Day Mortality
ATHOS-3: No significant mortality difference (46% vs 54%, P=0.12). Study not powered for mortality. Post-hoc AKI/RRT subgroup: 53% vs 30% survival (P=0.012). Mortality benefit uncertain.
none
A
Thromboembolic Events
SAFETY CONCERN: ATHOS-3: 13% vs 5% thromboembolic events (DVT, arterial). Major imbalance in DVT. Concurrent DVT prophylaxis required. Systematic review (n=1,461): Similar rates in larger observational data (8.8% vs 9.4% VTE).
moderate↓Worsens
B
Cardiac Protection
5 human trials support this finding. Human clinical trial data available.
small↑Improves
C
Kidney Function
10 preclinical studies support this finding. Primarily preclinical evidence.
moderate↑Improves
C
Blood Pressure
6 preclinical studies support this finding. Primarily preclinical evidence.
small↓Improves
D
Anti-Cancer Activity
2 preclinical studies support this finding. Primarily preclinical evidence.
small↑Improves
D
Muscle Mass/Function
2 preclinical studies support this finding. Primarily preclinical evidence.
small↑Improves
D
Cancer Cell Apoptosis
2 preclinical studies support this finding. Primarily preclinical evidence.
small↑Improves
D
Anti-Inflammatory Activity
2 preclinical studies support this finding. Primarily preclinical evidence.
small↑Improves
B
Renal Recovery in AKI
Post-hoc ATHOS-3 (n=105): Higher RRT liberation rate and 28-day survival (53% vs 30%, P=0.012) in AKI patients. May preferentially benefit those with renal failure. Requires prospective validation.
moderate↑Improves