A-779 (10⁻¹⁰ to 10⁻⁶ M) can competitively bind to Mas-transfected CHO cells with an IC50 of 0.3 nM [2]. A-779 (10⁻⁸ M; pre-incubated for 10 min, then incubated with Ang-(1-7) at 37°C for 15 min) TFA can block Ang-(1-7)-induced release of [3H]-arachidonic acid in Mas-transfected CHO and COS cells [2].

A-779 (24 μg/kg/h; intravenous injection; continuous infusion; 8 days) TFA significantly increased urine output in unmated female Sprague Dawley rats by 126%[1]. A-779 (24 μg/kg/h; intravenous injection; continuous infusion; from 8 days before pregnancy to 19 days of pregnancy) TFA significantly reduced food intake by 83% and urine output by 76% in late pregnancy Sprague Dawley rats, and reduced water intake by 83% and 80% in mid and late pregnancy, respectively, without affecting fetal outcome[1]. Continuous intravenous infusion of A-779 TFA at a rate of 80 ng/min significantly attenuated the enhancing effect of captopril on bradykinin hypotensive effects in conscious male Wistar rats[3]. A-779 (48 µg/kg; intravenous injection; single dose; 100 pM; co-incubation with isolated aortic rings) TFA partially blocked the Ang-(1-7)-induced hypotensive response in male Dahl salt-sensitive rats with high salt-induced hypertension and inhibited all Ang-(1-7)-mediated changes in vasodilatory/vasoconstrictive prostaglandin, nitric oxide and cGMP levels [4].

Animal/Disease Models:Sprague Dawley (female, 9 weeks old) [1]
Doses: 24 μg/kg/h
Route of Administration: Intravenous injection; continuous infusion; 8 days
Experimental Results: Urine output increased by 126%. Urine osmolality showed a decreasing trend. Compared with the solvent control group, feed consumption and water intake were not changed.

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Animal/Disease Models:Sprague Dawley (female, originally 9 weeks old and unmated, now pregnant)[1]
Doses: 24 μg/kg/h
Route of Administration: Intravenous injection; continuous infusion; from 8 days before pregnancy to 19 days of gestation
Experimental Results: Compared with the solvent control group, water intake decreased by 83% in mid-pregnancy (day 15 of gestation). Compared with the solvent control group, feed consumption decreased by 83%, water intake decreased by 80%, and urine output decreased by 76% in late pregnancy (day 19 of gestation). Urine osmolality tended to increase in late pregnancy. No significant effects were observed on fluid/food intake-excretion balance, urinary sodium or potassium concentration, maternal weight, or fetal characteristics (weight, length, number).

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Animal/Disease Models:Wistar mice (male, 230-320 g) [3]
Doses: 80 ng/min
Route of Administration: Intravenous injection; continuous infusion
Experimental Results: Significantly altered the dose-response curve of intravenously injected bradykinin, requiring approximately twice the dose of captopril alone to achieve the same antihypertensive effect. Significantly weakened the enhancing effect of captopril on the antihypertensive effect of intra-arterial bradykinin. When bradykinin was infused alone (without captopril), it did not significantly alter the antihypertensive effect of bradykinin or the baseline mean arterial pressure. It did not alter the pressor effect of angiotensin II. It did not alter the inhibitory effect of captopril on the pressor response of angiotensin I. It did not alter the decrease in baseline mean arterial pressure caused by captopril.

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Animal/Disease Models:Dahl salt-sensitive rats (male, 4-5 weeks old, high-salt diet 8.0% NaCl for 2 weeks or low-salt diet 0.3% NaCl) [4]
Doses: 48 µg/kg (in vivo); 100 pmol (in vitro tissue incubation)
Route of Administration: Intravenous injection; single dose (in vivo); incubation with isolated aortic rings (in vitro)
Experimental Results: Blocked the 14 mmHg decrease in maximum mean arterial pressure induced by Ang-(1-7) in high-salt diet rats, thus significantly attenuating the decrease in blood pressure. Prevented the Ang-(1-7)-induced increase in plasma 6-keto-PGF1α levels, maintaining them at near-baseline levels. Prevented the Ang-(1-7)-induced decrease in plasma TXB2 levels, maintaining them at near-baseline levels. It prevented Ang-(1-7)-induced increases in plasma nitric oxide levels, maintaining them at near-baseline levels. It also prevented Ang-(1-7)-induced increases in aortic ring 6-keto-PGF1α levels (from 31 pg/mL/mg ring weight to 49 pg/mL/mg ring weight, then maintained at 36 pg/mL/mg ring weight) and PGE2 levels (from baseline 22 pg/mL/mg ring weight to Ang-(1-7)-induced 33 pg/mL/mg ring weight, then maintained at 21 pg/mL/mg ring weight) in high-salt diet rats. In high-salt diet rats, Ang-(1-7) attenuated the Ang-(1-7)-induced decrease in aortic ring TXB2 levels (from baseline 44 pg/mL/mg ring weight to Ang-(1-7)-induced 23 pg/mL/mg ring weight, then increased to 37 pg/mL/mg ring weight). Ang-(1-7) prevented the increase in nitric oxide levels in the aortic ring of rats on both high- and low-salt diets. Ang-(1-7) completely eliminated the 52% increase in cGMP levels in the aortic ring of high-salt rats (from a baseline level of 102 fmol/mg protein to an Ang-(1-7)-induced level of 212 fmol/mg protein, and maintained at 67 fmol/mg protein). Compared with baseline values in both diet groups, there were no significant effects on MAP, plasma 6-keto-PGF1α, TXB2, nitric oxide, aortic ring 6-keto-PGF1α, PGE2, TXB2, nitric oxide, or cGMP levels.

[1]. Administration of D-Alanine-[Ang-(1-7)] (A-779) Prior to Pregnancy in Sprague Dawley Rats Produces Antidiuresis in Late Gestation. J Am Soc Hypertens. 2008;2(6):425-430.

[2]. Angiotensin-(1-7) is an endogenous ligand for the G protein-coupled receptor Mas. Proc Natl Acad Sci U S A. 2003;100(14):8258-8263.

[3]. Angiotensin-(1-7) antagonist A-779 attenuates the potentiation of bradykinin by captopril in rats. J Cardiovasc Pharmacol. 2004;43(5):685-691.

[4]. 1A-779 attenuates angiotensin-(1-7) depressor response in salt-induced hypertensive rats. Peptides. 2002;23(1):57-64.

C41H61F3N12O13

986.99

Asp-Arg-Val-Tyr-Ile-His-{d-Ala}DRVYIH-{d-Ala}

DRVYIH-{d-Ala}

Typically exists as solids at room temperature

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)