Catalogue Number
AV-P11479
Analysis Method
HPLC,NMR,MS
Specification
98%
Storage
2-8°C
Molecular Weight
175.19
Appearance
White crystalline powder
Botanical Source
Trichosanthes kirilowii Maxim.
Structure Type
Amino Acid/Peptides
Category
Standards;Natural Pytochemical;API
SMILES
C(CC(C(=O)O)N)CNC(=O)N
Synonyms
(2S)-2-amino-5-(carbamoylamino)pentanoic acid/L-(+)-Citrulline/α-amino-δ-ureidovaleric acid/Sitrulline/N5-(Aminocarbonyl)ornithine/d-ureidonorvaline/(S)-2-Amino-5-ureidopentanoic acid/N-Carbamoylornithine/anti-citrulline/N-[Hydroxy(imino)methyl]-L-ornithine/L-2-Amino-5-ureidovaleric acid/δ-Ureidonorvaline/[14C]-Citrulline/(S)-2-Amino-5-ureidopentanoic acid L-2-Amino-5-ureidovaleric acid/L(+)-Citrulline/L-Cytrulline/2-amino-5-(carbamoylamino)pentanoic acid/Nd-Carbamylornithine/N5-(Aminocarbonyl)-L-ornithine/2-Amino-5-ureidovaleric acid/Nδ-Carbamylornithine/L-N5-carbamoyl-Ornithine/L-Citrulline/N-Carbamoyl-L-ornithine/2-amino-5-(aminocarbonylamino)pentanoic acid/N-(aminocarbonyl)ornithine/Citrulline/L-Ornithine, N5- (aminocarbonyl)-/Ornithine, N-(aminocarbonyl)-/a-Amino-d-ureidovaleric Acid/L-citrulline zwitterion/N(5)-(aminocarbonyl)-DL-ornithine/N5-(aminocarbonyl)-Ornithine/L-Ornithine, N-(hydroxyiminomethyl)-/N5-carbamylornithine/L-Ornithine, N-(aminocarbonyl)-/N5-Carbamoyl-L-ornithine/N5-carbamoylornithine/(S)-2-amino-5-(carbamoyl amino)pentanoic acid/Ornithine, N5-(aminocarbonyl)-/H-Cit-OH
IUPAC Name
(2S)-2-amino-5-(carbamoylamino)pentanoic acid
Density
1.3±0.1 g/cm3
Solubility
Aqueous acid; Water
Flash Point
187.7±27.9 °C
Boiling Point
386.7±42.0 °C at 760 mmHg
Melting Point
214 °C
InChl
InChl Key
WGK Germany
RID/ADR
HS Code Reference
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:372-75-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
No Technical Documents Available For This Product.
27749691 q
Purpose of review: L-Citrulline, either synthetic or in watermelon, may improve vascular function through increased L-arginine bioavailability and nitric oxide synthesis. This article analyses potential vascular benefits of L-citrulline and watermelon supplementation at rest and during exercise.
Recent findings: There is clear evidence that acute L-citrulline ingestion increases plasma L-arginine, the substrate for endothelial nitric oxide synthesis. However, the subsequent acute improvement in nitric oxide production and mediated vasodilation is inconsistent, which likely explains the inability of acute L-citrulline or watermelon to improve exercise tolerance. Recent studies have shown that chronic L-citrulline supplementation increases nitric oxide synthesis, decreases blood pressure, and may increase peripheral blood flow. These changes are paralleled by improvements in skeletal muscle oxygenation and performance during endurance exercise. The antihypertensive effect of L-citrulline/watermelon supplementation is evident in adults with prehypertension or hypertension, but not in normotensives. However, L-citrulline supplementation may attenuate the blood pressure response to exercise in normotensive men.
Summary: The beneficial vascular effects of L-citrulline/watermelon supplementation may stem from improvements in the L-arginine/nitric oxide pathway. Reductions in resting blood pressure with L-citrulline/watermelon supplementation may have major implications for individuals with prehypertension and hypertension. L-Citrulline supplementation, but not acute ingestion, have shown to improve exercise performance in young healthy adults.
Influence of L-citrulline and Watermelon Supplementation on Vascular Function and Exercise Performance
Arturo Figueroa 1 , Alexei Wong, Salvador J Jaime, Joaquin U Gonzales
2017 Jan 12
29415069
L-citrulline and L-arginine supplementation has been shown to have several beneficial effects on the cardiovascular system. Nitric oxide (NO) protects against the progression of atherosclerosis and is synthesized by nitric oxide synthase (NOS), which converts L-arginine (L-Arg) into L-citrulline (L-Cit). Our previous study revealed that chronic administration of a combination of L-Cit and L- Arg has a better therapeutic effect on high cholesterol-induced atherosclerosis in rabbits. We investigated how L-Arg and L-Cit affect endothelial function, aging and atherosclerosis. Following a 3-day stimulation of human umbilical venous endothelial cells (HUVECs) with high glucose (HG: 22 mM) and L-Arg (300 μM), L-Cit (300 μM) or L-Arg plus L-Cit (LALC: each 150 μM) supplementation, endothelial senescence and function were evaluated. These amino acids were also administered to dyslipidemic type 2 diabetic (ZDFM) rats fed a high cholesterol diet. They were fed L-Arg or L-Cit or LALC for four weeks. Aortic senescence was investigated by measuring senescence-associated ß-galactosidase (SA-ß-gal), telomerase activity, DNA damage and p16INK4a protein expression. Only L-Cit and LALC supplementation retarded the HG-induced endothelial senescence, as evaluated by SA-ß-gal activity, a widely used marker of cellular senescence, p16INK4a expression, a senescence-related protein, and DNA damage. Under HG conditions, L-Cit and LCLA restored telomerase activity to levels observed under normal glucose (NG) conditions. Under HG conditions, L-Cit decreased ROS production, as measured by CM-H2DCFDA and the expression of p67phox, a major component of NADPH oxidase. Under HG conditions, L-Cit and LALC increased NO production, as measured by DAF-2AM. Endothelial NO synthase (eNOS) and phosphorylated eNOS were decreased under HG conditions and L-Cit and LALC significantly increased these levels. Arginase 2 protein expression increased under the HG conditions, and L-Cit and LALC significantly attenuated this effect. In ZDFM rats, SA-ß-gal activity was detected on the aortic endothelial surface; however, L-Cit and LALC reduced these levels. L-Cit and LALC both decreased the proportion of senescent cells. Furthermore, treatment with LALC for 4 weeks increased plasma NO production. Therefore conclusively, L-citrulline supplementation rescued NO levels better than L-arginine supplementation by inhibiting ROS production and arginase 2 protein expression. Consequently, L-Cit and LCLA supplementation retaeded HG-induced endothelial senescence.
Administration of L-arginine Plus L-citrulline or L-citrulline Alone Successfully Retarded Endothelial Senescence
Tomoe Tsuboi 1 2 , Morihiko Maeda 1 , Toshio Hayashi 1
2018 Feb 7
30284051
Purpose of review: Several interventional studies assessed the impact of dietary supplements on blood pressure. The aim of the present systematic review and meta-analysis was to determine the efficacy of L-citrulline supplementation on blood pressure.
Recent finding: Pubmed, Scopus, Google Scholar, and ISI Web of Science were comprehensively searched until May 2018 to assess whether L-citrulline reduces blood pressure. Human clinical trials which reported the effect of L-citrulline supplementation on aortic and brachial blood pressure were included. Characteristics of studies and potential sources of heterogeneity were tabulated. A subgroup analysis was performed to attenuate observed inter-study heterogeneity. A total of five interventions were found for meta-analysis. The impact of L-citrulline on brachial systolic (change 0.28 mmHg; 95% CI – 2.87, 2.31 mmHg) and diastolic (change – 1.56 mmHg; 95% CI – 4.32, 1.20 mmHg) blood pressure was not significant. Also, there was no changes in aortic systolic (change 0.22 mmHg; 95% CI – 4.81, 4.38 mmHg) and diastolic (change 0.26 mmHg; 95% CI – 2.27, 2.80 mmHg) blood pressure after L-citrulline supplementation. Participants’ body weight status was a source of observed heterogeneity. The present systematic review and meta-analysis suggests that L-citrulline supplementation had no beneficial effect on blood pressure.
Blood pressure; L-citrulline; Meta-analysis; Systematic review.
Effect of L-Citrulline Supplementation on Blood Pressure: A Systematic Review and Meta-Analysis of Clinical Trials
Mohammad Sadegh Mirenayat 1 , Sajjad Moradi 2 , Hamed Mohammadi 1 , Mohammad Hossein Rouhani 3
2018 Oct 3