Angiotensin 1-7: Cardiovascular Peptide Research

Angiotensin 1-7 (Ang 1-7) is a seven-amino-acid peptide that sits at the center of one of medicine's most important control systems: the renin-angiotensin system (RAS). While most people have heard of angiotensin II — the peptide that raises blood pressure and drives heart disease — far fewer know about its molecular opposite. Ang 1-7 is what happens when the body converts angiotensin II into something protective. It dilates blood vessels instead of constricting them. It reduces inflammation instead of amplifying it. It protects the heart and kidneys instead of stressing them.

This peptide represents a counter-regulatory arm of the RAS, and research has linked it to cardiovascular protection, kidney health, metabolic function, and even COVID-19 pathophysiology. The enzyme that produces it — ACE2 — is the same receptor SARS-CoV-2 uses to infect cells, which brought unprecedented attention to this peptide during the pandemic.

Understanding angiotensin 1-7 means understanding how the body balances opposing forces: constriction versus dilation, inflammation versus healing, damage versus repair. This article translates the science behind Ang 1-7 into something accessible — what it is, how it works, what the research shows, and where therapeutic development stands.

Quick Facts
What Is Angiotensin 1-7?
The Renin-Angiotensin System: A Balancing Act
How Angiotensin 1-7 Works
Research Applications
COVID-19 Connection
Clinical Development
Safety Profile
Legal and Regulatory Status
Frequently Asked Questions
Bottom Line

Quick Facts

Property	Details
Full Name	Angiotensin-(1-7)
Type	Heptapeptide (seven amino acids)
Sequence	Asp-Arg-Val-Tyr-Ile-His-Pro (DRVYIHP)
Molecular Weight	899.01 g/mol
Receptor	Mas receptor (MasR), also shows biased agonism at AT1R
Precursor	Angiotensin II (converted by ACE2)
Key Enzyme	ACE2 (angiotensin-converting enzyme 2)
Function	Vasodilation, anti-inflammatory, anti-fibrotic, cardioprotective
RAS Axis	Counter-regulatory (protective) arm

What Is Angiotensin 1-7?

Angiotensin 1-7 is an endogenous peptide hormone — a short chain of amino acids that your body produces naturally as part of blood pressure regulation and cardiovascular homeostasis. The sequence is Asp-Arg-Val-Tyr-Ile-His-Pro, which distinguishes it from angiotensin II by the absence of one amino acid (phenylalanine) at the C-terminus.

Where angiotensin II is known for raising blood pressure and promoting cardiovascular stress, Ang 1-7 does the opposite. It acts through the Mas receptor to produce vasodilation, reduce oxidative stress, inhibit fibrosis, and protect tissues from inflammatory damage. This makes it a counter-regulatory peptide — one that balances and opposes the effects of angiotensin II.

The peptide was first characterized in the 1980s, but its biological importance wasn't fully recognized until researchers identified ACE2 as its primary synthetic enzyme and the Mas receptor as its target in the early 2000s. Since then, Ang 1-7 has been studied in contexts ranging from heart failure and hypertension to diabetes, kidney disease, cancer, and most recently, COVID-19.

The Renin-Angiotensin System: A Balancing Act

To understand angiotensin 1-7, you need a basic map of the renin-angiotensin system. This is the body's main blood pressure control network, but it does far more than regulate fluid balance. It affects inflammation, oxidative stress, tissue remodeling, and cellular growth.

The RAS has two opposing sides:

The Classical (Pressor) Arm

This is the side most medical students learn first:

Renin is released by the kidneys in response to low blood pressure
Angiotensin I is produced from angiotensinogen
ACE (angiotensin-converting enzyme) converts Ang I into Angiotensin II
Angiotensin II binds to AT1 receptors, causing:
- Vasoconstriction (narrowing of blood vessels)
- Sodium retention (raising blood pressure)
- Inflammation and oxidative stress
- Fibrosis (scarring in heart, kidney, and blood vessels)
- Cell proliferation and hypertrophy

This arm is protective in acute situations — bleeding, dehydration, shock — where raising blood pressure saves lives. But chronic overactivation drives cardiovascular disease, kidney failure, and metabolic dysfunction.

The Counter-Regulatory (Depressor) Arm

This is where angiotensin 1-7 fits:

ACE2 converts angiotensin II into Angiotensin 1-7
Angiotensin 1-7 binds to Mas receptors, causing:
- Vasodilation (relaxing blood vessels)
- Natriuresis (sodium excretion, lowering blood pressure)
- Anti-inflammatory effects
- Anti-fibrotic effects (preventing scarring)
- Inhibition of cell proliferation and oxidative stress

ACE2 also converts angiotensin I into angiotensin-(1-9), which can be further processed into Ang 1-7. Other enzymes like neprilysin (NEP) and thimet oligopeptidase (TOP) can generate Ang 1-7 from Ang I as well, though ACE2 is the dominant pathway.

The balance between these two arms determines cardiovascular health. Overactive classical RAS (too much Ang II) leads to hypertension, heart failure, and kidney disease. Boosting the Ang 1-7 axis can counteract this damage.

This is why ACE inhibitors and angiotensin receptor blockers (ARBs) — drugs that block the Ang II pathway — are so widely prescribed. But targeting Ang 1-7 directly represents a newer strategy that's still being explored in clinical trials.

How Angiotensin 1-7 Works

Angiotensin 1-7 exerts its effects primarily through the Mas receptor, a G protein-coupled receptor (GPCR) discovered in the early 2000s. When Ang 1-7 binds to Mas, it triggers a cascade of intracellular signals that oppose angiotensin II's actions.

Mas Receptor Signaling

Binding of Ang 1-7 to the Mas receptor activates several protective pathways:

Nitric oxide (NO) release: Ang 1-7 stimulates endothelial nitric oxide synthase (eNOS), producing NO, which relaxes blood vessels and improves blood flow
Bradykinin potentiation: Ang 1-7 inhibits ACE, slowing the breakdown of bradykinin and amplifying its vasodilatory effects
Anti-inflammatory signaling: Reduces expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and adhesion molecules
Antioxidant effects: Decreases NADPH oxidase (NOX4) expression and reactive oxygen species (ROS) production
Anti-fibrotic actions: Inhibits TGF-β signaling and promotes matrix metalloproteinase (MMP) activity, preventing collagen accumulation

Research shows that Ang 1-7 also acts as a biased agonist at the AT1 receptor — the same receptor that Ang II uses to cause vasoconstriction. But when Ang 1-7 binds, it activates only the β-arrestin pathway (which is protective) without triggering G protein signaling (which causes vasoconstriction and inflammation). This dual mechanism — Mas activation plus AT1 bias — explains much of its cardioprotective profile.

Cardiovascular Protection

Ang 1-7 protects the cardiovascular system through multiple mechanisms:

Reduces cardiac hypertrophy: Prevents the thickening of heart muscle that occurs in hypertension and heart failure
Inhibits cardiac fibrosis: Blocks collagen deposition in the heart, preserving contractile function
Improves endothelial function: Restores normal blood vessel responsiveness, reducing arterial stiffness
Decreases atherosclerosis: Reduces plaque formation by limiting oxidative stress and inflammation in arterial walls
Prevents arrhythmias: Improves electrical conduction and cell-to-cell communication in heart tissue

In animal models, chronic Ang 1-7 infusion prevents hypertension-induced cardiac remodeling and improves outcomes in heart failure. Studies using genetic overexpression of ACE2 (which boosts Ang 1-7 levels) show similar protective effects.

Kidney Protection

The kidneys are both a source and target of RAS peptides. Ang 1-7 protects kidney function by:

Reducing glomerular damage and proteinuria (protein in urine)
Inhibiting renal fibrosis and slowing progression to chronic kidney disease
Improving glomerular filtration through vasodilation of renal blood vessels
Decreasing oxidative stress and inflammation in kidney tissue

In diabetic kidney disease models, Ang 1-7 treatment reduces albuminuria and slows the decline in kidney function, suggesting therapeutic potential in diabetic nephropathy.

Metabolic Effects

Beyond cardiovascular protection, Ang 1-7 influences glucose and lipid metabolism:

Improves insulin sensitivity: Modulates insulin receptor signaling in adipose tissue and skeletal muscle
Reduces visceral fat: Decreases adipocyte size and total fat mass
Lowers triglycerides: Improves lipid profiles in metabolic syndrome models
Improves glucose tolerance: Reduces fasting glucose and enhances glucose clearance

In fructose-fed rats (a model of metabolic syndrome), chronic Ang 1-7 treatment reduced body weight by 9.5%, decreased triglycerides by 51%, and improved insulin sensitivity. This suggests that targeting the ACE2/Ang 1-7/Mas axis could be useful in treating obesity-related metabolic disorders.

Research Applications

Angiotensin 1-7 has been studied across a broad range of preclinical and clinical contexts. Here's where the evidence stands.

Hypertension and Heart Failure

The strongest research base exists for cardiovascular applications. In rodent models of hypertension, Ang 1-7 infusion lowers blood pressure through sustained vasodilation. It also prevents the cardiac remodeling that occurs in chronic hypertension — the left ventricular hypertrophy, fibrosis, and diastolic dysfunction that eventually lead to heart failure.

Genetic studies support this. Mice lacking the Mas receptor develop exaggerated hypertension and cardiac damage when challenged with Ang II infusion. Conversely, overexpressing ACE2 or chronically administering Ang 1-7 protects against heart failure in animal models.

ACE2 and Ang 1-7 have been proposed as therapeutic targets for both heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). While ACE inhibitors and ARBs already provide some benefit by reducing Ang II levels, direct Ang 1-7 administration or ACE2 augmentation could offer additional protection, particularly in patients with overactive RAS.

Diabetic Complications

Diabetes accelerates cardiovascular and renal disease through multiple mechanisms, many of which involve RAS dysregulation. Research shows that diabetes shifts the RAS balance toward Ang II dominance, with reduced ACE2 expression and lower Ang 1-7 levels.

In diabetic animal models, Ang 1-7 treatment:

Prevents diabetes-induced cardiac dysfunction
Reduces kidney damage and proteinuria
Improves insulin signaling in peripheral tissues
Lowers blood glucose and improves glucose tolerance

Human studies remain limited, but epidemiological data suggest that people with diabetes benefit more from RAS-blocking drugs (ACE inhibitors and ARBs) than would be predicted by blood pressure lowering alone, possibly because these drugs shift the balance toward Ang 1-7.

Atherosclerosis and Vascular Disease

Ang 1-7 reduces atherosclerosis in apolipoprotein E-knockout (ApoE-KO) mice, a standard model of plaque formation. Treatment activates Mas receptors in vascular endothelium, stimulates nitric oxide production, and reduces inflammatory cytokine expression — all of which slow plaque development.

The peptide also inhibits vascular smooth muscle cell proliferation and migration, processes that contribute to arterial narrowing after injury (as in restenosis following angioplasty). This positions Ang 1-7 as a potential anti-proliferative agent in vascular disease.

Pulmonary Arterial Hypertension

The lungs contain a local RAS, and pulmonary arterial hypertension (PAH) — a disease characterized by high blood pressure in lung blood vessels — involves Ang II-driven vasoconstriction and remodeling. Research shows that ACE2 and Ang 1-7 protect against PAH in animal models.

In rats treated with monocrotaline (MCT), a toxin that induces PAH, Ang 1-7 infusion or ACE2 overexpression significantly reduced right ventricular systolic pressure and prevented pulmonary vascular remodeling. Similar protective effects were seen in bleomycin-induced lung fibrosis models.

The synthetic Ang 1-7 analog TXA-127 is currently in clinical trials for PAH, testing whether boosting this pathway can improve outcomes in human patients.

Cancer Research

Ang 1-7 has demonstrated anti-cancer properties in preclinical models. The peptide inhibits proliferation of human cancer cell lines in vitro and reduces tumor growth in xenograft mouse models.

Mechanisms include:

Anti-angiogenic effects (blocking new blood vessel formation that feeds tumors)
Inhibition of cell proliferation through cell cycle arrest
Induction of apoptosis (programmed cell death) in cancer cells
Reduction of metastatic spread

A phase II clinical trial tested subcutaneous Ang 1-7 (20 mg daily) in patients with metastatic sarcoma. While the cancer biomarker endpoints were not met, some patients experienced prolonged disease stabilization, suggesting potential utility in combination therapies or specific cancer types.

Metabolic Syndrome

The ACE2/Ang 1-7/Mas axis modulates lipid and glucose metabolism and counteracts many features of metabolic syndrome. In fructose-fed rats, chronic Ang 1-7 treatment improved multiple metabolic parameters:

Reduced body weight and visceral fat
Lowered serum triglycerides by 51%
Improved glucose tolerance and insulin sensitivity
Reduced blood pressure

In obese mice, oral administration of Ang 1-7 improved metabolic profiles and favorably altered intestinal microbiota composition, suggesting gut-mediated effects. This opens the possibility of oral Ang 1-7 formulations for metabolic disease, though peptide stability in the GI tract remains a challenge.

Inflammatory and Infectious Disease

Ang 1-7 has broad anti-inflammatory properties. It reduces expression of pro-inflammatory cytokines and adhesion molecules, which play roles in sepsis, acute lung injury, and chronic inflammatory diseases.

In a Mycoplasma pneumoniae infection model, Ang 1-7 treatment reduced inflammation and pathogen burden in mouse lungs. The peptide's ability to modulate immune responses without causing immunosuppression makes it attractive for conditions where excessive inflammation drives tissue damage.

COVID-19 Connection

The COVID-19 pandemic brought ACE2 and angiotensin 1-7 into the spotlight. SARS-CoV-2, the virus that causes COVID-19, infects cells by binding to ACE2. This creates a paradox: ACE2 is the entry point for the virus, but it's also part of a protective system that generates Ang 1-7.

ACE2 Downregulation and Disease Severity

When SARS-CoV-2 binds to ACE2, it internalizes the receptor, effectively removing it from the cell surface. This reduces ACE2 activity, which has two consequences:

Less angiotensin II is converted to Ang 1-7
Angiotensin II accumulates, driving inflammation, vasoconstriction, and coagulation

Studies of hospitalized COVID-19 patients show dysregulated RAS peptide levels. Some research found decreased Ang 1-7 levels inversely correlated with disease severity — patients with lower Ang 1-7 had worse outcomes, more inflammation, and higher rates of thrombosis. Other studies found paradoxically elevated Ang 1-7 in severe cases, possibly reflecting a compensatory but inadequate response to ACE2 loss.

The consensus is that COVID-19 disrupts the Ang II/Ang 1-7 balance in favor of Ang II, contributing to the cytokine storm, acute respiratory distress syndrome (ARDS), and thrombotic complications seen in severe cases.

Clinical Trials of Angiotensin 1-7 in COVID-19

Several trials tested whether supplementing Ang 1-7 could mitigate COVID-19 severity:

A phase 1-2 trial in ICU patients tested continuous IV infusion of Ang 1-7 at up to 10 mcg/kg/day for seven days. The peptide was safe and showed signals of reduced inflammation and improved oxygenation, though larger trials are needed to confirm efficacy.
A randomized pilot trial tested TXA-127 (synthetic Ang 1-7) at 0.5 mg/kg/day IV in 24 patients with severe COVID-19. No serious adverse events occurred, but the small sample size limited conclusions about effectiveness.
Larger trials using TXA-127 and another Ang 1-7 analog (TRV-027) in 35 U.S. sites did not show improvement in oxygen-free days compared to placebo, suggesting that Ang 1-7 supplementation alone may not be sufficient to alter COVID-19 outcomes. However, patient selection, dosing, and timing may have affected results.

Despite mixed clinical results, the biological rationale for Ang 1-7 in COVID-19 remains strong, and it may find use in specific patient subgroups or in combination with other therapies.

Clinical Development

While Ang 1-7 has strong preclinical evidence for cardiovascular, metabolic, and renal protection, translation to approved therapies has been slow. Here's where development stands.

Challenges in Drug Development

Angiotensin 1-7 faces several obstacles as a therapeutic:

Short half-life: Like most peptides, Ang 1-7 is rapidly degraded by circulating peptidases, requiring continuous infusion or frequent dosing
Route of administration: Peptides generally can't be taken orally because they're digested in the stomach
Clinical trial complexity: Cardiovascular outcomes trials require large patient populations and long follow-up periods
Regulatory hurdles: Peptide drugs face stringent manufacturing and stability requirements

These challenges have pushed researchers toward developing Ang 1-7 analogs with improved stability and bioavailability.

Angiotensin 1-7 Analogs

Several modified versions of Ang 1-7 are in development:

TXA-127: A synthetic, pharmaceutically formulated version of Ang 1-7 tested in clinical trials for COVID-19, pulmonary arterial hypertension, muscular dystrophy, and chemotherapy-induced myelosuppression. At 100 mcg/kg, it improved platelet counts in cancer patients receiving chemotherapy.
DSC127 (NorLeu3-Ang 1-7): A metabolically stable analog in phase III trials for diabetic foot ulcers. It's applied topically to accelerate wound healing.
HPβCD/Ang 1-7: A cyclodextrin-complexed formulation that improves peptide stability and allows for oral administration. Early studies in rodents show improved metabolic outcomes.
Cyclic Ang 1-7: A modified version with enhanced resistance to enzymatic degradation.
AVE-0991: A non-peptide Mas receptor agonist that mimics Ang 1-7 effects without being a peptide, potentially allowing oral dosing.

Phase I Safety Data

A phase I trial of subcutaneous Ang 1-7 in cancer patients established a recommended phase II dose of 400 mcg/kg. At 700 mcg/kg, dose-limiting toxicities occurred, including stroke (grade 4) and reversible cranial neuropathy (grade 3). At the recommended dose, the peptide was well-tolerated with minimal adverse effects.

In the COVID-19 trials, IV infusion up to 10 mcg/kg/day was safe, with no drug-related serious adverse events. This suggests a therapeutic window exists, though careful dose optimization is needed.

Future Directions

Despite limited clinical success to date, interest in Ang 1-7 therapeutics remains high. Potential applications include:

Heart failure (both HFrEF and HFpEF)
Hypertension resistant to current therapies
Diabetic nephropathy and cardiovascular complications
Pulmonary arterial hypertension
Metabolic syndrome and obesity
Acute lung injury and ARDS

Gene therapy approaches using AAV vectors to deliver ACE2 or Ang 1-7 are also being explored in preclinical models, offering the possibility of sustained peptide production without repeated injections.

Safety Profile

Angiotensin 1-7 appears relatively safe based on animal studies and early-phase clinical trials, though data remain limited.

Preclinical Safety

Toxicological studies in two animal species supported progression to human trials. Chronic infusion in rodents at doses producing cardiovascular effects did not cause significant toxicity. The peptide is an endogenous hormone, which generally reduces the risk of immune reactions or off-target effects.

Clinical Safety

In phase I cancer trials, Ang 1-7 was well-tolerated up to 400 mcg/kg subcutaneously. Higher doses (700 mcg/kg) caused neurological adverse events, suggesting a dose ceiling.

In COVID-19 trials, continuous IV infusion up to 10 mcg/kg/day for seven days produced no serious adverse events. Patients receiving TXA-127 at 0.5 mg/kg/day also tolerated the treatment without significant toxicity.

Potential Risks

Theoretical concerns include:

Hypotension: Ang 1-7 is a vasodilator, so excessive dosing could lower blood pressure too much
Kidney effects in certain contexts: One study in rats with subtotal nephrectomy found adverse cardiac effects from exogenous Ang 1-7, which were prevented by ACE inhibition. This suggests that in some forms of kidney disease, the balance of RAS peptides needs careful management.
Drug interactions: Combining Ang 1-7 with other RAS-targeting drugs (ACE inhibitors, ARBs, direct renin inhibitors) could amplify effects, requiring dose adjustments.

Long-term safety data from chronic use are not yet available, so questions about extended treatment remain open.

Legal and Regulatory Status

Angiotensin 1-7 is not FDA-approved as a therapeutic agent. It remains a research peptide with investigational status.

Current Regulatory Standing

United States: Ang 1-7 and its analogs (TXA-127, DSC127) are in clinical trials but have not received FDA approval for any indication.
Europe: Similar status — research-stage compounds without marketing authorization.
Other regions: No approved formulations exist globally as of early 2025.

Research Use

Ang 1-7 is available from biochemical suppliers for laboratory research. It is not legally available for human use outside of approved clinical trials.

Comparison to Angiotensin II

Interestingly, angiotensin II (not Ang 1-7) received FDA approval in December 2017 for treatment of septic and distributive shock. This highlights a regulatory asymmetry: the peptide that raises blood pressure has been developed as a drug, while the one that lowers it has not yet crossed the approval threshold.

Future Outlook

If ongoing trials demonstrate efficacy in conditions like diabetic foot ulcers (DSC127) or pulmonary arterial hypertension (TXA-127), the first Ang 1-7-based drugs could reach the market in the next few years. Until then, the peptide remains confined to research and experimental medicine.

Frequently Asked Questions

Is angiotensin 1-7 the same as angiotensin II?

No. Both are peptides in the renin-angiotensin system, but they have opposite effects. Angiotensin II raises blood pressure, causes vasoconstriction, and promotes inflammation and fibrosis. Angiotensin 1-7 lowers blood pressure, causes vasodilation, and has anti-inflammatory and anti-fibrotic effects. Ang 1-7 is actually produced from Ang II by the enzyme ACE2.

Can you take angiotensin 1-7 as a supplement?

No. Angiotensin 1-7 is a research peptide with no approved formulations for human use. It is not available as a supplement and should only be administered in clinical trials under medical supervision. Peptides taken orally are typically digested before they can be absorbed, so even if available, oral consumption would be ineffective without special formulations.

Does angiotensin 1-7 lower blood pressure?

Yes, in research models. Angiotensin 1-7 produces vasodilation and sodium excretion (natriuresis), both of which lower blood pressure. In animal studies, chronic Ang 1-7 infusion reduces blood pressure in hypertensive models. However, clinical trials testing this in humans have not yet been completed.

What is the relationship between ACE2 and angiotensin 1-7?

ACE2 (angiotensin-converting enzyme 2) is the enzyme that produces angiotensin 1-7 from angiotensin II. This makes ACE2 the key switch that shifts the renin-angiotensin system from its pro-inflammatory, vasoconstrictive side (Ang II) to its protective, vasodilatory side (Ang 1-7). Boosting ACE2 activity increases Ang 1-7 levels and provides cardiovascular protection in research models.

Why did COVID-19 affect angiotensin 1-7 levels?

SARS-CoV-2 infects cells by binding to the ACE2 receptor. This binding internalizes and degrades ACE2, reducing its enzymatic activity. With less ACE2 available, less angiotensin II is converted to angiotensin 1-7, leading to an imbalance: too much Ang II (causing inflammation, vasoconstriction, and clotting) and too little Ang 1-7 (which normally counteracts these effects). This imbalance contributes to severe COVID-19 complications.

Can angiotensin 1-7 help with heart failure?

Potentially. Preclinical research shows that Ang 1-7 prevents and reverses cardiac remodeling in animal models of heart failure. It reduces cardiac hypertrophy, fibrosis, and inflammation while improving heart function. Clinical trials are needed to determine whether these benefits translate to human patients with heart failure.

Is angiotensin 1-7 being tested in clinical trials?

Yes. Angiotensin 1-7 and its analogs (TXA-127, DSC127) have been tested in trials for COVID-19, cancer, diabetic foot ulcers, pulmonary arterial hypertension, and muscular dystrophy. DSC127 is in phase III trials for diabetic wound healing. Results have been mixed, with some showing safety but limited efficacy. Development continues.

What is the Mas receptor?

The Mas receptor (MasR) is a G protein-coupled receptor that angiotensin 1-7 binds to produce its biological effects. When Ang 1-7 activates Mas, it triggers vasodilation, nitric oxide release, anti-inflammatory signaling, and anti-fibrotic pathways. The Mas receptor is found in blood vessels, heart, kidneys, brain, and other tissues, explaining Ang 1-7's broad protective effects.

Bottom Line

Angiotensin 1-7 represents a shift in how scientists think about the renin-angiotensin system. For decades, the focus was on blocking angiotensin II — the "bad actor" that drives hypertension, heart failure, and kidney disease. ACE inhibitors and ARBs work by reducing Ang II or preventing it from binding to receptors.

But angiotensin 1-7 reframes the problem. Instead of just removing the harmful peptide, the body actively produces a protective one from it. ACE2 converts Ang II into Ang 1-7, which then activates the Mas receptor to undo the damage. This is not just suppression — it's active counter-regulation.

The research base is strong. In animal models, Ang 1-7 protects the heart from hypertrophy and fibrosis, shields the kidneys from diabetic damage, improves metabolic dysfunction, reduces atherosclerosis, and mitigates lung injury. Mechanistically, it works through vasodilation, nitric oxide release, anti-inflammatory signaling, and inhibition of fibrotic pathways.

The challenge is translation. Peptides are difficult drugs. They're unstable, require injection, and degrade quickly. Early clinical trials have shown safety but modest efficacy, and no Ang 1-7-based drug has reached FDA approval yet. Analogs like TXA-127 and DSC127 aim to solve these problems with improved stability and alternative formulations, and phase III trials are underway.

COVID-19 added urgency to this field. The virus hijacks ACE2, disrupting the Ang II/Ang 1-7 balance and contributing to severe disease. While Ang 1-7 infusion trials in COVID-19 patients showed safety, efficacy results were mixed, suggesting that supplementing the peptide alone may not be enough to reverse viral-induced RAS dysregulation.

For now, angiotensin 1-7 remains a research peptide — not yet a drug, but a promising target. If development succeeds, it could offer a new class of cardiovascular, metabolic, and anti-inflammatory therapies. Until then, the science continues to clarify how the body uses this peptide to protect itself, and how medicine might learn to amplify that protection.

Disclaimer: This article is for educational purposes only and does not constitute medical advice. Angiotensin 1-7 is not FDA-approved for any medical use and should not be used outside of approved clinical trials. Consult a licensed healthcare provider before making decisions about cardiovascular or metabolic health treatments.

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