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Catalogue Number : BF-M3018
Specification : 98%
CAS number : 315-22-0
Formula : C16H23NO6
Molecular Weight : 325.36
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystal

Botanical Source

Crotalaria pallida

Structure Type



Standards;Natural Pytochemical;API




Monocrotaline/crotaline/Monccrotalire/Bulbus Lilii/CROTALINE/(13a,14a)-14,19-Dihydro-12,13-dihydroxy-20-norcrotolanan-11,15-dione/Monocrotaline/2H-[1,6]Dioxacycloundecino[2,3,4-gh]pyrrolizine-2,6(3H)-dione, 4,5,8,10,12,13,13a,13b-octahydro-4,5-dihydroxy-3,4,5-trimethyl-, (3R,4R,5R,13aR,13bR)-/(3R,4R,5R,13aR,13bR)-4,5-Dihydroxy-3,4,5-trimethyl-4,5,8,10,12,13,13a,13b-octahydro-2H-[1,6]dioxacycloundecino[2,3,4-gh]pyrrolizine-2,6(3H)-dione/MONOCRATALINE/A 6080/MONOCROTALIN/CROTALIN/Crotaline,Monocrotaline




1.4±0.1 g/cm3


Flash Point

278.7±30.1 °C

Boiling Point

537.3±50.0 °C at 760 mmHg

Melting Point

204ºC (dec.)(lit.)


InChl Key

WGK Germany


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#:315-22-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Background: Monocrotaline has been widely used to establish an animal model of pulmonary hypertension. The molecular target underlying monocrotaline-induced pulmonary artery endothelial injury and pulmonary hypertension remains unknown. The extracellular calcium-sensing receptor (CaSR) and particularly its extracellular domain hold the potential structural basis for monocrotaline to bind. This study aimed to reveal whether monocrotaline induces pulmonary hypertension by targeting the CaSR.
Methods and results: Nuclear magnetic resonance screening through WaterLOGSY (water ligand-observed gradient spectroscopy) and saturation transfer difference on protein preparation demonstrated the binding of monocrotaline to the CaSR. Immunocytochemical staining showed colocalization of monocrotaline with the CaSR in cultured pulmonary artery endothelial cells. Cellular thermal shift assay further verified the binding of monocrotaline to the CaSR in pulmonary arteries from monocrotaline-injected rats. Monocrotaline enhanced the assembly of CaSR, triggered the mobilization of calcium signaling, and damaged pulmonary artery endothelial cells in a CaSR-dependent manner. Finally, monocrotaline-induced pulmonary hypertension in rats was significantly attenuated or abolished by the inhibitor, the general or lung knockdown or knockout of CaSR.
Conclusions: Monocrotaline aggregates on and activates the CaSR of pulmonary artery endothelial cells to trigger endothelial damage and, ultimately, induces pulmonary hypertension.


endothelial injury; extracellular calcium-sensing receptor; intracellular calcium; monocrotaline; pulmonary hypertension.


Monocrotaline Induces Endothelial Injury and Pulmonary Hypertension by Targeting the Extracellular Calcium-Sensing Receptor


Rui Xiao 1 2 , Yuan Su 2 3 , Tian Feng 1 2 , Mengxiang Sun 1 2 , Bingxun Liu 1 2 , Jiwei Zhang 2 4 , Yankai Lu 2 5 , Jiansha Li 2 5 , Tao Wang 2 6 , Liping Zhu 7 2 , Qinghua Hu 7 2 8

Publish date

2017 Mar 22




Purpose/Aim: Low doses (30-80 mg/kg) of monocrotaline are commonly used to create experimental models of pulmonary hypertension in rats. At these doses, monocrotaline causes pulmonary endothelial apoptosis and acute lung injury which ultimately results in pulmonary vascular disease. Higher doses of monocrotaline (300 mg/kg) are known to create severe liver injury, but previous investigations with lower doses have not reported histology in other organs to determine whether the vascular injury with monocrotaline is pulmonary-selective or generalized.
Materials and methods: We therefore sought to determine whether monocrotaline caused extra-pulmonary injury at doses commonly used in pulmonary hypertension studies. We performed left pneumonectomy on young male and female rats before administering 50-60 mg/kg monocrotaline 7 days later. We monitored serum chemistry and urine dipsticks during the first 3 weeks while the animals developed pulmonary hypertension. After 3 weeks, we sacrificed animals and stained the lungs and highly vascular visceral organs (kidney, liver, and spleen) for elastin to evaluate the degree of vascular injury and remodeling.
Results: We did not observe proteinuria or significant transaminitis over the 3 weeks following monocrotaline. As previously published, monocrotaline caused severe pulmonary vascular disease with neointimal lesions and medial hypertrophy. We did not identify significant large or small arterial damage in the kidneys, liver, or spleen. Two external veterinary pathologists did not identify histopathology in the kidneys, liver, or spleen of these rats.
Conclusions: We conclude that 50-60 mg/kg of monocrotaline causes a selective pulmonary vascular lesion and that male and female rats have little non-pulmonary damage over 3 weeks at these doses of monocrotaline.


endothelial injury; extracellular calcium-sensing receptor; intracellular calcium; monocrotaline; pulmonary hypertension.


Low Dose Monocrotaline Causes a Selective Pulmonary Vascular Lesion in Male and Female Pneumonectomized Rats


Daniel J Lachant 1 2 , David F Meoli 1 2 , Deborah Haight 1 2 , Jason A Lyons 1 2 , Robert F Swarthout 1 2 , R James White 1 2

Publish date

2018 Feb




Aims: This study aims to explore the molecular mechanisms underlying sphingosine kinase 1 (SphK1) inducing pulmonary vascular remodeling and resveratrol suppressing pulmonary arterial hypertension (PAH).
Material and methods: monocrotaline (MCT) was used to induce PAH in rats. The right ventricular systolic pressure (RVSP), right ventricle hypertrophy index (RVHI) and histological analyses including hematoxylin and eosin staining, the percentage of medial wall thickness (%MT), α-SMA staining and Ki67 staining were performed to evaluate the development of PAH. Protein levels of SphK1, nuclear factor-kappaB (NF-κB)-p65 and cyclin D1 were determined using immunoblotting. Sphingosine-1-phosphate (S1P) concentration was measured using enzyme-linked immunosorbent assay.
Key findings: SphK1 protein level, S1P production, NF-κB activation and cyclin D1 expression were significantly increased in MCT-induced PAH rats. Inhibition of SphK1 by PF543 suppressed S1P synthesis and NF-κB activation and down-regulated cyclin D1 expression in PAH rats. Suppression of NF-κB by pyrrolidine dithiocarbamate (PDTC) also reduced cyclin D1 expression in PAH model. Treatment of PAH rats with either PF543 or PDTC dramatically decreased RVSP, RVHI and %MT and reduced pulmonary arterial smooth muscle cells proliferation and pulmonary vessel muscularization. In addition, resveratrol effectively inhibited the development of PAH by suppression of SphK1/S1P-mediated NF-κB activation and subsequent cyclin D1 expression.
Significance: SphK1/S1P signaling induces the development of PAH by activation of NF-κB and subsequent up-regulation of cyclin D1 expression. Resveratrol inhibits the MCT-induced PAH by targeting on SphK1 and reverses the downstream changes of SphK1, indicating that resveratrol might be a therapeutic agent for the prevention of PAH.


Pulmonary hypertension; Resveratrol; Sphingosine kinase 1; Vascular remodeling.


Resveratrol Inhibits Monocrotaline-Induced Pulmonary Arterial Remodeling by Suppression of SphK1-mediated NF-κB Activation


Wenhua Shi 1 , Cui Zhai 2 , Wei Feng 1 , Jian Wang 1 , Yanting Zhu 2 , Shaojun Li 2 , Qingting Wang 2 , Qianqian Zhang 2 , Xin Yan 2 , Limin Chai 2 , Pengtao Liu 2 , Yuqian Chen 2 , Manxiang Li 3

Publish date

2018 Oct 1