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Catalogue Number : BD-D1316
Specification : 98%(HPLC)
CAS number : 51014-29-0
Formula : C22H26N2O4
Molecular Weight : 382.45
PUBCHEM ID : 3037448
Volume : 20MG

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Uncaria rhynchophylla(Miq.)Miq. ex Havil./Alkaloid from Uncaria attenuata attenuata and Mitragyna rotundifolia (Naucleaceae)

Structure Type



Standards;Natural Pytochemical;API




Methyl (16E,20α)-16-(methoxymethylene)-2-oxocorynox-18-en-17-oate/Y0112/17-methoxy-2-oxo-corynoxa-16,18-diene-16-carboxylic acid methyl ester/Spiro[3H-indole-3,1'(5'H)-indolizine]-7'-acetic acid, 6'-ethenyl-1,2,2',3',6',7',8',8'a-octahydro-α-(methoxymethylene)-2-oxo-, methyl ester, (αE,3S,6'R,7'S,8'aS)-/Isocorynoxeine/cisocorynoxeine


methyl (E)-2-[(3S,6'R,7'S,8'aS)-6'-ethenyl-2-oxospiro[1H-indole-3,1'-3,5,6,7,8,8a-hexahydro-2H-indolizine]-7'-yl]-3-methoxyprop-2-enoate


1.3±0.1 g/cm3



Flash Point

294.1±30.1 °C

Boiling Point

562.7±50.0 °C at 760 mmHg

Melting Point



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#:51014-29-0) 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.




This study was designed to investigate the vasorelaxant effects and underlying mechanism of isocorynoxeine (ICN), one of the indole alkaloids from Uncaria hooks, on isolated mesenteric arteries in vitro. The myograph system was applied for isometric tension recording in the vascular rings. ICN relaxed both endothelium-intact and endothelium-denuded rat vascular rings precontracted with phenylephrine or KCl in a dose-dependent manner. Propranolol, tetraethylammonium, BaCl2, and glibenclamide had no influence on the vasodilator effect of ICN on phenylephrine-primed vascular rings, while 4-aminopyridine decreased the maximum relaxation. Furthermore, ICN produced a significant drop in maximum response in the PE log concentration-response curve without shifting to the right. In the Ca2+-free Kreb’s-Henseleit buffer, ICN inhibited the contraction in vascular rings evoked by PE, but not by KCl. The phasic contractions of segments in the Ca2+-free Kreb’s-Henseleit buffer induced by CaCl2 were restrained by ICN, while contractions elicited by caffeine displayed no differences. Furthermore, the phasic vasodilation of ICN was significantly lower than controls when pretreated with nifedipine and heparin. Both BAYK8644- and PE-evoked responses were significantly inhibited in the presence of 100 μM of ICN in human vascular smooth muscle cells loaded with the fluorescent Ca2+ indicator Fluo-4-AM. All these results suggest that ICN act in an endothelium-independent manner on the mesenteric artery. Its mechanisms of vasorelaxant action were produced by the inhibition of L-type calcium channel-mediated external Ca2+ influx and α1A-adrenoceptor-mediated intracellular Ca2+ release in vascular smooth muscle cells, and the participation of the Kv channel.


Calcium channel; Isocorynoxeine (ICN); Rat mesenteric artery; Vasorelaxation; α1A-Adrenoceptor antagonist


Endothelium-independent vasodilator effect of isocorynoxeine in vitro isolated from the hook of Uncaria rhynchophylla (Miquel).


Li T1,2, Xu K1,2, Che D1,3, Huang Z4, Jahan N1,2, Wang S5,6.

Publish date

2018 Nov




Isocorynoxeine, one of the major alkaloids from Uncaria Hook, shows the effects of lowering blood pressure, vasodilatation, and protection against ischemia-induced neuronal damage. In this paper, the metabolism of isocorynoxeine was investigated in rats. Twelve metabolites and the parent drug were isolated by using solvent extraction and repeated chromatographic methods, and determined by spectroscopic methods including UV, MS, NMR, and CD experiments. Seven new compounds were identified as 11-hydroxyisocorynoxeine, 5-oxoisocorynoxeinic acid-22-O-β-D-glucuronide, 10-hydroxyisocorynoxeine, 17-O-demethyl-16,17-dihydro-5-oxoisocorynoxeine, 5-oxoisocorynoxeinic acid, 21-hydroxy-5-oxoisocorynoxeine, and oxireno[18, 19]-5-oxoisocorynoxeine, together with six known compounds identified as isocorynoxeine, 18,19-dehydrocorynoxinic acid, 18,19-dehydrocorynoxinic acid B, corynoxeine, isocorynoxeine-N-oxide, and corynoxeine-N-oxide. Possible metabolic pathways of isocorynoxeine are proposed. Furthermore, the activity assay for the parent drug and some of its metabolites showed that isocorynoxeine exhibited a significant neuroprotective effect against glutamate-induced HT22 cell death at the maximum concentration. However, little or weak neuroprotective activities were observed for M-3, M-6, M-7, and M-10. Our present study is important to further understand their metabolic fate and disposition in humans.

Georg Thieme Verlag KG Stuttgart · New York.


Isolation and identification of twelve metabolites of isocorynoxeine in rat urine and their neuroprotective activities in HT22 cell assay.


Qi W1, Chen F1, Sun J2, Simpkins JW2, Yuan D1.

Publish date

2015 Jan




Medical therapy of lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH) targets smooth muscle contraction in the prostate, for which α1A-adrenoceptor (α1A-AR) antagonists have been considered to be the primary therapeutic method. We investigated the effects and underlying mechanisms of isocorynoxeine (ICN), one of indole alkaloids from Uncaria, on the treatment of LUTS secondary to BPH via α1A-ARs in mice. The effect of ICN on prostatic contractility was studied via myographic measurements in the prostates of rabbits. The effects of ICN on bladder function, serum-hormone levels, bladder histology, and prostate histology were determined in testosterone propionate-induced prostatic hyperplasic wild-type (WT) and α1A-AR knockout (α1A-KO) mice. The cytotoxicity of ICN in cultured human prostatic stromal cells (WPMY-1) was assessed by the following: a cell-counting kit, measuring the relaxant effect on WPMY-1 by a collagen gel contraction assay, intracellular Ca2+ mobilization indicated by Fluo-4, cytoskeletal organization by phalloidin staining, and expressions of α1A-AR-mediated key messengers by western blot analyses. ICN non-competitively antagonized the contractions of prostates induced by α1A-AR agonists. ICN treatment improved bladder functions in prostatic hyperplasic WT mice, whereas it failed to ameliorate bladder functions in prostatic hyperplasic α1A-KO mice. In WPMY-1, ICN relaxed cell contractions on collagen gels, disrupted F-actin organization, inhibited α1A-AR agonist-stimulated Ca2+ mobilization, and antagonized α1A-ARs via the RhoA/ROCK2/MLC signaling pathway. Our results suggest that ICN may be a promising therapeutic drug for targeting α1A-ARs in the treatment of BPH/LUTS.

Copyright © 2019 Elsevier Inc. All rights reserved.


Benign prostatic hyperplasia; Isocorynoxeine; Lower urinary tract symptoms; α(1A)-Adrenoceptor


Effects of isocorynoxeine, from Uncaria, on lower urinary tract dysfunction caused by benign prostatic hyperplasia via antagonism of α1A-adrenoceptors.


Li T1, Xu K1, He J1, Jahan N1, Song J2, Wang S3.

Publish date

2019 Aug 1