Angiotensin-(1-7)

Ang-(1-7), A(1-7); TXA127 (a pharmaceutical formulation); NorLeu³-A(1-7) / DSC127 is a modified analogue

Cardiovascular & circulation

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Naturally occurring heptapeptide (7 amino acids) of the renin–angiotensin system, formed mainly when ACE2 clips one residue off angiotensin II
Mechanism: Acts chiefly at the Mas receptor to oppose angiotensin II: widening vessels, reducing fibrosis and inflammation, and limiting cell proliferation
Routes studied: Intravenous and subcutaneous infusion (human studies); topical gel as the analogue DSC127 (wound trials); intranasal and oral formulations explored preclinically
Half-life: Seconds to a few minutes in plasma — degraded by ACE and other peptidases. This is the central reason it has never become a practical drug
Storage: Research peptide; lyophilised, cold storage. Not a consumer product
Regulatory status: Not approved anywhere for any indication

Doses are as reported in studies or by the community — never recommendations.

1What it is

Most people know the renin–angiotensin system through its pressure-raising arm: renin makes angiotensin I, ACE converts it to angiotensin II, and angiotensin II constricts vessels, retains salt and drives fibrosis. That is the arm blocked by ACE inhibitors and ARBs.

Angiotensin-(1-7) belongs to the other arm. The enzyme ACE2 converts angiotensin II into this shorter peptide, which acts on a different receptor (Mas) and does roughly the opposite: vessels relax, fibrosis slows, inflammation falls. Part of the benefit of ACE inhibitors and ARBs is thought to come from shifting the system toward this branch. ACE2's second claim to fame — as the entry receptor for SARS-CoV-2 — is why this peptide received a burst of attention after 2020.

It is a research compound and a hospital-trial compound, not a self-administered one. Community use: essentially none documented, and the seconds-long makes informal use pointless.

2How it's thought to work

Binds the Mas receptor (MAS1), a G-protein-coupled receptor distinct from AT1 and AT2, triggering nitric-oxide and prostaglandin-mediated vasodilation.

Opposes AT1 receptor signalling functionally, and at high concentrations interacts with AT1 and AT2 directly.

Reduces fibrosis by lowering TGF-β and collagen deposition in heart, kidney and lung models.

Dampens NADPH-oxidase-driven oxidative stress and inflammatory cytokine production.

Stimulates haematopoietic progenitor cells, which is the basis for the trials in bone-marrow recovery.

Improves insulin signalling in rodent models of metabolic syndrome.

Angiotensin-(1-7) at the Mas receptor, the counter-regulatory arm of the same renin-angiotensin system. Where angiotensin II narrows the vessel, this widens it, and it opposes the fibrosis and growth signals of the AT1 arm.Schematic — not to scale

3What the research shows

Haematopoietic recovery after chemotherapy

TXA127 was studied for accelerating platelet and neutrophil recovery after cytotoxic chemotherapy and stem-cell transplant, on the basis that Ang-(1-7) stimulates progenitor cells. Early-phase studies reported biological activity and acceptable tolerability in small patient numbers (Rodgers and colleagues; Phase 1/2 reports in the 2000s). Never confirmed in a large randomised trial.

COVID-19 and ARDS

Several small randomised trials infused Ang-(1-7) in hospitalised COVID-19 patients, reasoning that the virus's consumption of ACE2 leaves the protective arm depleted. Results were mixed and sample sizes small; the largest reports did not establish benefit, and no product advanced (Wagener and colleagues; multiple 2021–2023 reports — individual trial details should be checked before citing †).

Graded A (negative)

Diabetic foot ulcers (topical analogue)

DSC127, a topical formulation of the stabilised analogue NorLeu³-A(1-7), reached Phase 3 for diabetic foot ulcer healing after encouraging Phase 2 data. The Phase 3 programme was discontinued for lack of efficacy †.

Human cardiovascular and renal physiology

Short infusions in healthy volunteers and hypertensive patients produce modest vasodilation and effects on renal sodium handling; effects are smaller and less consistent than in animals, partly because of the rapid breakdown (various small studies, 1990s–2010s).

Cardiac, renal and pulmonary protection

Large and fairly consistent rodent literature: less hypertrophy after infarction, less kidney fibrosis, less pulmonary hypertension, improved endothelial function.

Graded B/C

Cancer

A Phase 1 study of Ang-(1-7) in patients with advanced solid tumours reported tolerability and some disease stabilisation, on an anti-angiogenic rationale (Petty 2009, Clin Cancer Res). Not pursued to later-phase success. [4]

4Reported side effects and interactions

Literature-reported

Generally well tolerated in short human studies. Reported effects include mild hypotension, flushing and injection-site reactions. No long-term human safety data.

Community-reported

None. Not in self-directed use.

Theoretical. Hypotension when stacked on RAS-blocking medication; effects on haematopoiesis mean the consequences of chronic exposure on blood cell lines are unstudied; the proliferative effect on progenitor cells cuts both ways in anyone with a haematological malignancy.

Interactions. ACE inhibitors raise endogenous Ang-(1-7) levels by blocking its degradation, so combining them is pharmacologically additive. Additive blood-pressure lowering with any antihypertensive. No formal interaction studies.

Markers researchers commonly monitor

Study-protocol measures; there is no home-monitoring use case.

Marker	Why it's watched
Blood pressure	the expected pharmacological effect and the dose-limiting one.
Full blood count with differential and platelets	the haematopoietic effect is both the therapeutic hypothesis and the thing to watch.
Creatinine, eGFR, electrolytes	the kidney is a principal target organ of the RAS.
Plasma renin activity, angiotensin II and Ang-(1-7) levels	pathway engagement, in research settings with access to these assays.
hs-CRP or other inflammatory markers	the anti-inflammatory hypothesis.
Echocardiographic measures of remodelling	in cardiac studies, over months rather than days.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Not applicable as a consumer practice. Research and trial material is handled as a sterile preparation for infusion or administration in a clinical setting, and the extremely short plasma means that bolus self-administration would have no sustained pharmacological meaning. No calculator preset applies.

6Commonly studied alongside

Apelin (#152 — the other ACE2-linked counter-regulatory peptide), adrenomedullin (#151), natriuretic peptides. In the laboratory it is studied together with ACE2 activators and with AT2-receptor agonists as parts of the same protective axis.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Investigational; orphan designations have been granted for TXA127 in certain indications †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Not specifically listed by WADA; as an unapproved peptide it would fall under S0 if used. Check the current list

8Open questions

Can the peptide be stabilised or delivered well enough to matter clinically, or is the Mas receptor better addressed with a small molecule?
Did the COVID-19 trials fail on biology or on design and timing?
Does chronic Mas-receptor activation produce the anti-fibrotic benefit seen in rodents in humans?
What is the real contribution of this arm to the benefit of ACE inhibitors and ARBs?

9References

1Santos RAS et al. (2003). Angiotensin-(1-7) is an endogenous ligand for the G protein-coupled receptor Mas. Proc Natl Acad Sci USA. PubMed · DOI
2Santos RAS et al. (2018). The renin–angiotensin system: going beyond the classical paradigms. Am J Physiol Heart Circ Physiol. PubMed · DOI
3Rodgers KE et al. (2006). Development of angiotensin (1-7) as an agent to accelerate dermal repair. Wound Repair Regen [verify]. PubMed
4Petty WJ et al. (2009). Phase I and pharmacokinetic study of angiotensin-(1-7), an endogenous antiangiogenic hormone. Clin Cancer Res. PubMed · DOI
5Ferrario CM, Chappell MC (2004). Novel angiotensin peptides. Cell Mol Life Sci. PubMed · DOI
6Wagener G et al. (2022). Angiotensin-(1-7) in severe COVID-19 — randomized trial report. Crit Care / Chest [verify journal and outcome]. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

forum threads →

community protocols include this →

Threads and protocols are visible to members. Joining is free.

Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

30 Oct 2026Profile published — awaiting medical review

Licensed CC BY-NC-SA 4.0. Found an error? Report it · Editorial standards — corrections are logged here.