Aminoguanidine HCL 75mg/ml , 60ml

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  • Product Code:AG60
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  • $32.00


Aminoguanidine is an AGE reducer and belongs to the class of chemicals known as AGE breakers/AGE inhibitors.  It is also known as pimagedine.  AGEs, advanced glycation end-products, result from the process of glycation, which is similar to caramelization.  It occurs when a lipid and glucose molecule bind together and is found in exogenous (outside the body) sources as well as manufactured inside the body as a result of cellular processes.  Diabetic hyperglycemia and other disease processes can result in higher levels of AGEs.  AGEs take 120 days or more to be excreted from the body; if greater-than-normal production occurs, high levels of AGEs cause many issues by cross-bonding proteins inappropriately: neuropathy, diabetic nephropathy, diabetes-related ED, and may also be implicated in degenerative chronic brain disorders such as Alzheimer’s. 

Aminoguanidine has been demonstrated to successfully treat diabetic nephropathy:

Hyperglycaemia is directly involved in causing long-term diabetic complications. The non-enzymatic glycation of proteins, yielding irreversible advanced glycation end products and advanced glycation end products-derived protein crosslinking, participates in the development of diabetic complications, such as diabetic nephropathy. Diabetic nephropathy is becoming a major medical problem with increasing numbers of these patients progressing to end stage renal disease, thus requiring renal replacement therapy. While several interventions may slow the development and progression of diabetic nephropathy, there is no effective treatment to prevent or reverse the disease. Pimagedine (aminoguanidine HCl) has been shown to be an effective agent in reducing the severity of the structural and functional alterations associated with experimental diabetic nephropathy. Preliminary studies suggest a beneficial effect of pimagedine in treating patients with diabetic nephropathy. In summary, these observations support a role for advanced glycation end products inhibitors, like pimagedine, in the management of diabetic nephropathy, either alone or in combination with other therapies.[1]

Di Naso et al found that in an experimental rat diabetes model, aminoguanidine reduced oxidative stress as well as disease-related tissue alterations:

We evaluated the effect of aminoguanidine on pulmonary oxidative stress and lung structure in an experimental model of diabetes mellitus. Thiobarbituric acid reactive substances (TBARS), histology and arterial blood gases were evaluated in animals with diabetes mellitus (DM group), animals with diabetes mellitus treated with aminoguanidine (DM+AG group), and controls. The TBARS levels were significantly higher in the DM group than in the control and DM+AG groups (2.90 ± 1.12 vs. 1.62 ± 0.28 and 1.68 ± 0.04 nmol/mg protein, respectively), as was PaCO2 when compared with that of the control group (49.2 ± 1.65 vs. 38.12 ± 4.85 mmHg), and PaO2 was significantly higher in the control group (104.5 ± 6.3 vs. 16.30 ± 69.48 and 97.05 ± 14.02 mmHg, respectively). In this experimental model of diabetes mellitus, aminoguanidine reduced oxidative stress, structural tissue alterations, and gas exchange.[2]

Aminoguanidine and AGE inhibitors are only one part of a comprehensive treatment plan; in modern diets high levels of AGEs are created by high-heat cooked, high-fat, high-sugar diets and have similar detrimental effects to the AGEs created by diseases. Reducing AGE intake is instrumental regardless of whether aminoguanidine or a similar treatment is administered:

Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.[3]

Aminoguanidine may help in treating certain injuries and related conditions through a mechanism unrelated to AGEs: inhibition of iNOS nitric oxide synthase:

BACKGROUND: This study was to delineate the therapeutic efficacy and potential cellular and molecular mechanisms of aminoguanidine (AG), a relatively selective inhibitor of iNOS activity, in cerebral vasospasm after subarachnoid hemorrhage (SAH) in rabbits….CTA data revealed that cerebral vasospasm of SAH rabbits was significantly prevented via AG treatment. TEM results demonstrated the ultrastructural morphological changes of endothelial cells of SAH rabbits were ameliorated by AG treatment. In parallel, AG treatment increased eNOS mRNA and protein levels along with the reduced immunoreactivity of nitrotyrosine in rabbit basilar arteries. CONCLUSIONS: Our discovery suggested AG inhibition of iNOS activity could significantly reverse cerebral vasospasm after SAH via restoration of dysfunctional endothelial cells by the upregulation of eNOS, indicating a regulatory cross-talk between eNOS and iNOS in the pathogenesis of SAH.[4]

Fan et al found that aminoguanidine helps improve motor function and other markers after spinal cord compression injury in rats, possibly through its antioxidant effects:

The current study was performed to investigate the effect of aminoguanidine (AG) on spinal cord injury (SCI) in rat. AG (75, 150 and 300mg/kg, i.p. respectively ) was administered to rats immediately following SCI. It was found that AG (150mg/kg) significantly reduced spinal cord water content and improved motor function, however, AG at the doses of 75 and 300mg/kg had no effect. Compared to SCI group without treatment, AG at the dosage of 150mg/kg induced a reduction in the permeability of blood-spinal cord barrier (BSCB) after injury 48h (from 59.8+/-5.5microl/g to 39.8+/-3.8microl/g), a 38% decrease of Malondialdehyde (MDA) values and a 1-fold increase of the Glutathione (GSH) levels at 12h after SCI. And the expression of inducible nitric oxide synthase (iNOS) protein reached a peak at 24h after injury, which was significantly attenuated by treatment with AG (150mg/kg). In addition, the expression of AQP4 protein was down-regulated by the treatment of AG (150mg/kg) at 24h after SCI, and the changes still lasted at 48h after injury. Our results indicated that AG could induce spinal cord edema clearance and improve motor function, which could be correlated with antioxidative property, the down-regulation of iNOS and AQP4 protein expression after SCI.[5]


[1] W Kline Bolton, Emaad Abdel-Rahman.  Pimagedine: a novel therapy for diabetic nephropathy.  April 2002, Vol. 11, No. 4 , Pages 565-574.

[2] Di Naso FC, Forgiarini Junior LA, Forgiarini LF, Porawski M, Dias AS, Marroni NA. Aminoguanidine reduces oxidative stress and structural lung changes in experimental diabetes mellitus.  J Bras Pneumol. 2010 Aug;36(4):485-9.

[3] Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, Yong A, Striker GE, Vlassara H. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010 Jun;110(6):911-16.e12.

[4] Zheng B, Zheng T, Wang L, Chen X, Shi C, Zhao S. Aminoguanidine inhibition of iNOS activity ameliorates cerebral vasospasm after subarachnoid hemorrhage in rabbits via restoration of dysfunctional endothelial cells.  J Neurol Sci. 2010 Aug 15;295(1-2):97-103.

[5] Fan ZK, Wang YF, Cao Y, Zhang MC, Zhang Z, Lv G, Lu W, Zhang YQ. The effect of aminoguanidine on compression spinal cord injury in rats.  Brain Res. 2010 Jun 25;1342:1-10.


*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.


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