D-NAME
D-NAME (NG-Nitro-D-arginine methyl ester) is an orally active enantiomer of L-NAME (HY-18729). D-NAME inhibits Nitric oxide synthase activity in myocardium and aorta (Note: D-NAME was once classified as an inactive substance and used as a negative control in nitric oxide synthase inhibition studies), induces increases in systolic blood pressure and mean arterial blood pressure, reduces mesenteric arterial conductance, elevates the ratio of left ventricular weight to body weight, induces myocardial fibrosis, increases the cross-sectional area of aortic wall, enhances mesenteric vasodilation induced by nitrovasodilators, and releases nitric oxide via its guanidino nitro group. D-NAME has no effect on ovalbumin-induced pulmonary eosinophilia in sensitized mice. D-NAME can be used in hypertension-related research.
For research use only. We do not sell to patients.
- CAS No.: 141968-19-6
- Formula: C7H15N5O4
- Molecular Weight:233.23
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
D-NAME releases NO, whereas L-Arginine (HY-N0455) or another NOS inhibitor L-NMMA (HY-18732) does not, which is consistent with the presence or absence of nitro groups in their structures and the nitro group's vasodilatory enhancing effect[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
D-NAME (50 mg/kg; i.p.; twice) does not inhibit OVA-induced pulmonary eosinophilia in sensitized male B6D2F1/J mice[2].
D-NAME (222 μmol/kg; i.p.; daily; 4 days) pretreatment potentiates nitrodilator (BDNIC, NTG)-mediated mesenteric vasodilation, increases mean arterial blood pressure, and decreases baseline mesenteric arterial conductance in female Sprague-Dawley rats[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, 15-week-old)[1]
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Dosage:40 mg/kg/day
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Administration:p.o.; daily; 4 weeks
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Result:Increased systolic blood pressure by 27% compared to controls after 4 weeks.
Reached a left ventricular weight-to-body weight ratio (LVW/BW) of 1.44 mg/g, representing a 13% increase compared to controls.
Elevated myocardial fibrosis to 5.25% of heart muscle area, up from 0.94% in controls.
Increased aortic wall cross-sectional area by 25% compared to controls.
Increased DNA concentration in the left ventricle and aorta significantly compared to controls.
Reduced myocardial NO synthase activity by 25% compared to controls, and reduced aortic NO synthase activity by 13% compared to controls.
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Animal Model:B6D2F1/J (male, 20-25 g, sensitized by i.p. injection of alum-precipitated ovalbumin, boosted 5 days later, then challenged with aerosolized ovalbumin twice in one day)[2]
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Dosage:50 mg/kg
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Administration:i.p.; twice (30 minutes before and 4 hours after first antigen challenge)
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Result:Had no effect on the increased number of eosinophils in the BAL fluid and peribronchial lung tissue induced by OVA challenge in sensitized mice.
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Animal Model:Sprague-Dawley (female, 301 g)[3]
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Dosage:222 μmol/kg
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Administration:i.p.; daily; 4 days
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Result:Potentiated mesenteric arterial vasodilation in response to BDNIC and NTG, increasing mesenteric conductance relative to control.
Increased mean arterial blood pressure.
Decreased baseline mesenteric arterial conductance.
Caused no change to plasma nitrite concentrations.
Chemical Information
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CAS No. 141968-19-6
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Molecular Weight 233.23
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Formula C7H15N5O4
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SMILES
N[C@H](CCCNC(N[N+]([O-])=O)=N)C(OC)=O
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Synonyms
NG-Nitro-D-arginine methyl ester
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Fibrosis/Collagen Morphometry
Fibrosis and collagen morphometry is based on the quantitative visualization of fibrillar collagen deposition in tissue sections using histochemical stains such as Sirius Red (Picrosirius Red) or Masson's trichrome, followed by image-based or polarization-enhanced analysis to estimate collagen proportional area as a surrogate of extracellular matrix accumulation during fibrotic remodeling. Sirius Red combined with polarized light microscopy enhances detection of collagen fibers due to birefringence properties, enabling more specific visualization of collagen type I and III fibrils compared to conventional bright-field histology, while whole-section or region-restricted digital morphometry reduces field-selection bias in fibrosis assessment. Alternative quantitative approaches include second harmonic generation (SHG) and two-photon excited fluorescence microscopy, which enable label-free detection of fibrillar collagen and have been validated against histological staining and biochemica
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Collagen: Sirius Red Staining
Sirius Red or picrosirius red staining is a histochemical method for visualizing collagen-rich extracellular matrix in tissue sections, and collagen fibers are detected as red-stained structures under bright-field microscopy with enhanced birefringence under polarized light. Picrosirius red is useful for assessing total collagen organization, distribution, and fibrosis burden, but polarized color should not be interpreted as a definitive collagen type I versus type III readout because color is affected by fiber orientation, thickness, and packing.
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Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
Masson’s Trichrome (collagen/trichrome staining) is a histological technique that differentially stains tissue compartments using sequential acidic dyes to distinguish collagen from muscle and cytoplasmic components based on dye affinity and tissue permeability differences, enabling visualization of fibrosis and connective tissue architecture in histological sections. The classical formulation typically uses Weigert's iron hematoxylin for nuclear staining, Biebrich scarlet-acid fuchsin for cytoplasm and muscle, and aniline blue (or light green variants) for collagen, producing a characteristic blue/green collagen signal contrasted against red cytoplasm and dark nuclei. The staining principle relies on selective displacement of smaller dye molecules by larger anionic dyes in collagen-rich regions under controlled acidified conditions, which enhances collagen-specific dye retention. This property makes the method widely used for fibrosis assessment in organs such as heart, liver, lung, a
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)