Angiotensin 1-7
Also known as: Ang-(1-7), Ang 1-7, Angiotensin-(1-7), Asp-Arg-Val-Tyr-Ile-His-Pro, TXA127
Endogenous heptapeptide; renin-angiotensin system (RAS) counter-regulatory peptide
What it is
Cardiovascular researchers and cardiologists study Angiotensin 1-7 as a naturally occurring peptide produced in the body that may counteract high blood pressure, heart disease, inflammation, and some cancers. It works by opposing the blood pressure-raising, vessel-narrowing effects of its cousin angiotensin II — relaxing blood vessels, reducing scarring, and calming inflammation. Not FDA-approved as a drug; active clinical trials are underway, and research surged after COVID-19 because the virus hijacks the enzyme that normally makes Angiotensin 1-7.
The scientific side
Angiotensin 1-7 (sequence: Asp-Arg-Val-Tyr-Ile-His-Pro) is a biologically active heptapeptide of the renin-angiotensin system (RAS) that functions as the primary counter-regulatory effector to Angiotensin II. It is generated from Angiotensin II by ACE2 (angiotensin-converting enzyme 2), or alternatively from Angiotensin I via the endopeptidases neprilysin, thimet oligopeptidase, and prolyl oligopeptidase (PMIDs: 9876288, 15962175, 24776703). Chronic use of ACE inhibitors raises plasma Ang 1-7 levels 10- to 25-fold, suggesting that part of the cardiovascular benefit of those drugs may be mediated through this peptide. Ang 1-7 acts on the G-protein-coupled Mas receptor expressed in the brain, heart, kidney, vasculature, and adipose tissue to produce effects broadly opposite to those of Angiotensin II: vasodilation, antihypertensive, antihypertrophic, antiatherogenic, antiarrhythmogenic, antifibrotic, and antithrombotic actions (PMIDs: 31602467, 19348228, 24664288). At the vascular level, it stimulates endothelial nitric oxide release and inhibits NADPH oxidase-related superoxide production, thereby reducing oxidative stress and improving endothelial function. In cardiac and vascular remodelling, Ang 1-7 antagonizes the AT1R-mediated cell growth, proliferation, migration, and oxidative stress pathways that drive heart failure and atherosclerosis. It reduces smooth muscle cell proliferation and migration, improves lipid metabolism, inhibits atherosclerotic lesion formation, and increases plaque stability. FGF21 has been shown to act on adipocytes and renal cells to upregulate ACE2, increasing Ang 1-7 production and thereby suppressing Angiotensin II-induced hypertension and vascular dysfunction in mice. In the adipose tissue, Ang 1-7 via the ACE2/Ang-(1-7)/Mas receptor axis counters pro-inflammatory adipokines and metabolic dysfunction associated with obesity. In skeletal muscle, Ang 1-7 (10 nM) counteracts Angiotensin II, improving satellite cell-mediated regeneration. In a murine pneumococcal pneumonia model, Ang 1-7 reduced lung inflammation, improved bacterial clearance, and enhanced survival, consistent with its known pro-resolving properties. In rheumatoid arthritis models, Ang 1-7 inhibited synovial angiogenesis and joint destruction via the Hippo-YAP pathway. The ACE2-Ang 1-7 axis is of particular importance in COVID-19 pathophysiology because SARS-CoV-2 uses ACE2 as its cellular entry receptor, thereby downregulating ACE2 expression and disrupting the protective Ang 1-7 pathway, contributing to cardiovascular and pulmonary complications (PMIDs: 24776703, 17293687).
Class: Endogenous heptapeptide; renin-angiotensin system (RAS) counter-regulatory peptide
Administration & storage
- Administration
- Intravenous infusion (human Phase I clinical trialsanimal studies)Subcutaneous injection (some animal studies)Intravenous bolus (mechanistic cardiovascular studies in rats)
- Storage
- As a peptide, Ang 1-7 is expected to require frozen storage (−20°C or below) for long-term stability, protected from repeated freeze-thaw cycles. Stability was specifically evaluated by HPLC in the Karal® antioxidant reperfusion formulation. Cyclodextrin encapsulation (TXA127) may improve ambient stability for oral forms. No specific storage conditions stated for injectables in the reviewed abstracts.
- Cautions
- Potent vasodilatory effects observed at pharmacological doses; risk of hypotension if given rapidly IV,Prostaglandin-dependent depressor responses observed in animal models; potential interaction with NSAIDs (indomethacin eliminated depressor response in rats, PMID: 8234010),Very short plasma half-life due to peptidase degradation — pharmacokinetic limitations noted as a barrier to clinical development,No human safety data available for subcutaneous self-administration; IV use restricted to clinical trial settings,SARS-CoV-2 / COVID-19 context: ACE2 downregulation by virus reduces endogenous Ang 1-7 production — therapeutic supplementation rationale but no approved use
Legal & regulatory status
Not FDA-approved as a therapeutic drug. Multiple investigational applications are active. TXA127 (an oral formulation of Angiotensin-(1-7) in hydroxypropyl-β-cyclodextrin) has been evaluated in Phase II trials including…
Not stated in reviewed literature — requires manual verification
Not stated in reviewed literature — requires manual verification
What it's studied for
- Hypertension and blood pressure regulation Mixed
- Comprehensive review establishing Ang 1-7 as a key antihypertensive component of the RAS, acting via Mas receptor-mediated vasodilation and opposing Ang II pressor actions. PMID 24664288 Santos RA et al., Hypertension (2014)
- In pithed rat models, intravenous Ang 1-7 produced a biphasic blood pressure response: a brief pressor phase followed by a dose-dependent depressor response (magnitude -4 to -13 mmHg; duration 83–255 seconds); the depressor component was prostaglandin-mediated and blocked by indomethacin. PMID 9876288 Iyer SN et al., Brazilian J Med Biol Res (1998)
- ACE inhibitor-induced 10- to 25-fold rise in plasma Ang 1-7 identified as likely mediator of antihypertensive benefit; multiple enzymatic pathways for Ang 1-7 generation described including ACE2. PMID 15962175 Sampaio WO et al., Cardiovascular Actions Review (2005)
- Review of translational cardiovascular evidence confirmed antihypertensive, antihypertrophic, antiatherogenic, antiarrhythmogenic, antifibrotic, and antithrombotic properties in animal models; noted paucity of human clinical data and pharmacokinetic limitations for therapeutic development. PMID 31602467 Patel VB et al., Am J Hypertension (2019)
- Phase I human clinical trial (now terminated) designed to assess vasodilatory effects of Ang 1-7 infusion in patients with essential hypertension. NCT02245230 — Cardiovascular Effects of Ang (1-7) in Essential Hypertension
- Cardiovascular remodelling, heart failure, and atherosclerosis Mixed
- Review of counter-regulatory RAS axis: Ang 1-7 via Mas receptor antagonizes AT1R-mediated cell growth, proliferation, migration, and oxidative stress driving cardiac and vascular remodelling; protective role in heart failure and atherosclerosis progression. PMID 24593683 Flores-Munoz M et al., Clinical Science (2014)
- Ang 1-7 reduces smooth muscle cell proliferation and migration, improves endothelial function and lipid metabolism, inhibits atherosclerotic lesion formation, and increases plaque stability in preclinical models. PMID 26788046 Jiang F et al., J Geriatric Cardiology (2015)
- Overview of ACE2/Ang 1-7 pathway protective effects in hypertension, atherosclerosis, myocardial remodelling, heart failure, ischaemic stroke, and diabetes mellitus from experimental and clinical studies; proposed as novel therapeutic target. PMID 24776703 Patel VB et al., Nature Reviews Cardiology (2014)
- Anti-inflammatory and immune-resolving effects (infection, arthritis, pneumonia) Animal studies only
- In a murine Streptococcus pneumoniae model, Ang 1-7 treatment reduced lung inflammation, improved bacterial clearance, and enhanced survival; combination with ceftriaxone showed synergistic benefit, consistent with pro-resolving anti-inflammatory properties. PMID 41296084 Oliveira AL et al., Inflammation Research (2025)
- In collagen-induced arthritis (CIA) mice, Ang 1-7 inhibited synovial angiogenesis and alleviated joint damage via suppression of the Hippo-YAP signalling pathway; arthritis scores and histopathology significantly improved. PMID 40955298 Zhang Y et al., J Inflammation Research (2025)
- Review showing Ang 1-7 counteracts pro-inflammatory adipokines in adipose tissue; increased ACE2/Ang-(1-7)/Mas axis activation associated with reduced metabolic inflammation and improved body homeostasis in obesity-associated disease states. PMID 30905634 Esteban V et al., Metabolism (2019)
- Cancer — chemotherapy hematologic support (thrombocytopenia and neutropenia protection) Phase II/III RCT
- Phase II completed clinical trial evaluating Ang 1-7 for prevention of chemotherapy-induced thrombocytopenia and neutropenia in patients receiving gemcitabine and carboplatin for ovarian, fallopian tube, or peritoneal cancer. NCT00771810 — Drug to Reduce Thrombocytopenia in Ovarian/Fallopian Cancer Patients on Chemotherapy
- Review of patent landscape identified cancer treatment as the most advanced therapeutic area for Ang 1-7, with clinical studies available in hematological indications alongside cardiovascular, transplantation, and surgical applications. PMID 27121991 Rodgers KE et al., Expert Opinion Therapeutic Patents (2016)
- Duchenne muscular dystrophy (DMD) cardiomyopathy — oral TXA127 formulation Phase II/III RCT
- Open-label Phase II multi-centre study of TXA127 (oral hydroxypropyl-β-cyclodextrin-encapsulated Ang 1-7) in non-ambulant patients with DMD-associated dilated cardiomyopathy; 6-month open-label treatment phase with efficacy endpoints. NCT06013839 — TXA127 in Non-Ambulant DMD Cardiomyopathy
- Ang 1-7 at 10 nM in C2C12 cell cultures counteracted Ang II-mediated impairment of satellite cell differentiation, improving skeletal muscle regeneration — supporting rationale for DMD applications. PMID 38112612 Oliveira AC et al., European J Translational Myology (2023)
- Skeletal muscle regeneration and muscular dystrophy Animal studies only
- In C2C12 myoblast cultures, 10 nM Ang 1-7 reversed Ang II-induced impairment of satellite cell differentiation and promoted muscle regeneration; diaphragm muscle studies provided supporting in vivo data. PMID 38112612 Oliveira AC et al., European J Translational Myology (2023)
- COVID-19 / SARS-CoV-2 supportive research (ACE2-RAS disruption hypothesis) Mechanistic only
- ACE2 is the key enzyme generating Ang 1-7 from Ang II; SARS-CoV-2 binds and downregulates ACE2, thereby reducing protective Ang 1-7 signalling — mechanistic basis for COVID-19-associated cardiovascular and pulmonary injury. PMID 24776703 Patel VB et al., Nature Reviews Cardiology (2014)
- Identification of ACE2 as the enzyme linking Ang II catabolism to Ang 1-7 production established the mechanistic basis for SARS-CoV-2 disruption of this pathway. PMID 17293687 Gallagher PE et al., Curr Op Nephrol Hypertension (2007)
- Metabolic disorders — obesity, diabetes, and vascular dysfunction Animal studies only
- FGF21 deficiency exacerbated Ang II-induced hypertension and vascular dysfunction in mice; FGF21 replenishment prevented this by upregulating ACE2 in adipocytes and renal cells, increasing Ang 1-7 levels and activating downstream anti-hypertensive signalling. PMID 29706566 Wan Z et al., Cell Metabolism (2018)
- Ang 1-7 counter-regulates pro-inflammatory adipokines in obesity; ACE2/Ang-(1-7)/Mas axis activation associated with reduced adipose inflammation and improved metabolic homeostasis. PMID 30905634 Esteban V et al., Metabolism (2019)
- Post-operative cognitive protection following coronary artery bypass surgery Mechanistic only
- Pilot case series evaluated perioperative Ang 1-7 for prevention of postoperative cognitive vulnerability following CABG surgery; hypothesis based on neurovascular protective and anti-inflammatory properties. Europe PMC preprint (2026), no PMID assigned
- Hepatocellular carcinoma — protective RAS axis Mechanistic only
- Review of protective RAS axis in hepatocellular carcinoma (HCC) identified ACE2/Ang 1-7 signalling as a potential therapeutic target to counter HCC progression and enhance response to existing therapies. Europe PMC preprint (2026), no PMID assigned
- Corneal injury repair (topical formulation research) Mechanistic only
- Ang 1-7-based proteomimetic polymers developed as topical agents for corneal repair following chemical injury; preclinical proof-of-concept study. Europe PMC preprint (2026), no PMID assigned
Safety signals
- Acute hypotension / blood pressure depression
- Very short plasma half-life — rapid peptidase degradation
- Potential NSAID interaction (prostaglandin pathway)
- Phase I trial termination (NCT02245230) — cardiovascular effects in hypertension
Contraindications
About these dose ranges
Dose ranges below reflect commonly reported community protocols. Where published research cites a specific dose, the PMID is linked. Doses without citations are not clinical recommendations — they reflect what practitioners and researchers commonly report using.
Community-reported dosing
| Route | Dose | Frequency / Duration | Population / context | Source tier |
|---|---|---|---|---|
| Cell culture medium | 10 nM | — | Study | Research PMID 38112612 |
| Intravenous injection (pithed rat model) | Dose-dependent range producing -4 to -13 mmHg depressor response over 83–255 seconds duration | — | Study | Research PMID 8234010 |
| Intravenous infusion | Not published in reviewed abstracts (Phase I dose-escalation) | — | Study | Research |
| Oral (hydroxypropyl-β-cyclodextrin encapsulation) | Not published in reviewed abstracts (Phase II) | — | Study | Research |
| Reperfusion solution (isolated heart model) | 50–5000 ng/mL validated range for HPLC-fluorescence analysis | — | Study | Research PMID 26452351 |
| Intravenous infusion (human clinical research) or subcutaneous (some animal studies); TXA127 oral formulation in Phase II trials | No established community dosing protocol. In research settings, IV infusion doses used in human trials are not disclosed in reviewed abstracts. Animal studies used 10 nM in cell culture and dose-dependent IV boluses producing -4 to -13 mmHg blood pressure effects (PMID: 8234010). | Not established for community use; clinical trials used variable infusion schedules | researchers and biohackers interested in cardiovascular health peptides; primarily a clinical trial agent with very limited community self-use documentation |
All studies (17)
- PMID 27121991 Phase II/III RCT
Cancer — chemotherapy hematologic support (thrombocytopenia and neutropenia protection) - PMID 38112612 Phase II/III RCT
Duchenne muscular dystrophy (DMD) cardiomyopathy — oral TXA127 formulation - PMID 9876288 Mixed
Hypertension and blood pressure regulation - PMID 15962175 Mixed
Hypertension and blood pressure regulation - PMID 24593683 Mixed
Cardiovascular remodelling, heart failure, and atherosclerosis - PMID 24664288 Mixed
Hypertension and blood pressure regulation - PMID 24776703 Mixed
Cardiovascular remodelling, heart failure, and atherosclerosis - PMID 26788046 Mixed
Cardiovascular remodelling, heart failure, and atherosclerosis - PMID 31602467 Mixed
Hypertension and blood pressure regulation - PMID 8234010
Dose-dependent range producing -4 to -13 mmHg depressor response over 83–255 seconds duration Intravenous injection (pithed rat model) () - PMID 17293687 Mechanistic only
COVID-19 / SARS-CoV-2 supportive research (ACE2-RAS disruption hypothesis) - PMID 26452351
50–5000 ng/mL validated range for HPLC-fluorescence analysis Reperfusion solution (isolated heart model) () - PMID 27456244
- PMID 29706566 Animal studies only
Metabolic disorders — obesity, diabetes, and vascular dysfunction - PMID 30905634 Animal studies only
Anti-inflammatory and immune-resolving effects (infection, arthritis, pneumonia) - PMID 40955298 Animal studies only
Anti-inflammatory and immune-resolving effects (infection, arthritis, pneumonia) - PMID 41296084 Animal studies only
Anti-inflammatory and immune-resolving effects (infection, arthritis, pneumonia)