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  • Brand : BIOFRON

  • Catalogue Number : BF-D3007

  • Specification : 98%

  • CAS number : 19408-84-5

  • Formula : C18H29NO3

  • Molecular Weight : 307.43

  • PUBCHEM ID : 107982

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Capsicum annuum

Structure Type



Standards;Natural Pytochemical;API




N-(4-Hydroxy-3-methoxybenzyl)-8-methylnonanamide/Nonanimidic acid, N-[(4-hydroxy-3-methoxyphenyl)methyl]-8-methyl-, (1Z)-/(1Z)-N-(4-Hydroxy-3-methoxybenzyl)-8-methylnonanimidic acid/6,7-Dihydrocapsaicin/8-methyl-nonanoic acid vanillylamide/N-[(4-Hydroxy-3-methoxy-phenyl)methyl]-8-methyl-nonanamide/Nonanamide,8-methyl-N-vanillyl/Dihydro Capsaicin/N-[(4-hydroxy-3-methoxyphenyl)methyl]-8-methylnonanamide/Nonanamide, N-[(4-hydroxy-3-methoxyphenyl)methyl]-8-methyl-/8-Methyl-N-vanillyl-nonamide/Dihydrocapsaicin/Nonanamide, 8-methyl-N-vanillyl-/8-Methyl-N-vanillylnonanamide/N-(4-hydroxy-3-methoxybenzyl)isodecanamide




1.0±0.1 g/cm3


Methanol; Ethyl Acetate

Flash Point

230.4±31.5 °C

Boiling Point

457.3±55.0 °C at 760 mmHg

Melting Point

62-65 °C(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#:19408-84-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




This study investigated the effect of dihydrocapsaicin (DHC) on cerebral and blood brain barrier (BBB) damage in cerebral ischemia and reperfusion (I/R) models. The models were induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. The rats were divided into five groups: sham, or control group; vehicle group; and 2.5 mg/kg, 5 mg/kg, and 10 mg/kg BW DHC-treated I/R groups. After 24 h of reperfusion, we found that DHC significantly reduced the area of infarction, morphology changes in the neuronal cells including apoptotic cell death, and also decreased the BBB damage via reducing Evan Blue leakage, water content, and ultrastructure changes, in addition to increasing the tight junction (TJ) protein expression. DHC also activated nuclear-related factor-2 (Nrf2) which involves antioxidant enzymes like superoxide dismutase (SOD) and glutathione peroxidase (GPx), and significantly decreased oxidative stress and inflammation via down-regulated reactive oxygen species (ROS), NADPH oxidase (NOX2, NOX4), nuclear factor kappa-beta (NF-ĸB), and nitric oxide (NO), including matrix metalloproteinases-9 (MMP-9) levels. DHC protected the cerebral and the BBB from I/R injury via attenuation of oxidative stress and inflammation. Therefore, this study offers to aid future development for protection against cerebral I/R injury in humans.


Dihydrocapsaicin Attenuates Blood Brain Barrier and Cerebral Damage in Focal Cerebral Ischemia/Reperfusion via Oxidative Stress and Inflammatory


Adchara Janyou 1 , Piyawadee Wicha 1 , Jinatta Jittiwat 2 , Apichart Suksamrarn 3 , Chainarong Tocharus 1 , Jiraporn Tocharus 4

Publish date

2017 Sep 5




Chili peppers are one of the most widely consumed spices worldwide. However, research on the health benefits of chili peppers and some of its constituents has raised controversy as to whether chili pepper compounds possess cancer-promoting or cancer-preventive effects. While ample studies have been carried out to examine the effect of capsaicin in carcinogenesis, the chemopreventive effect of other major components in chili pepper, including dihydrocapsaicin, capsiate, and capsanthin, is relatively unclear. Herein, we investigated the inhibitory effect of chili pepper components on malignant cell transformation. Among the tested chili pepper compounds, dihydrocapsaicin displayed the strongest inhibitory activity against epidermal growth factor (EGF)-induced neoplastic transformation. Dihydrocapsaicin specifically suppressed EGF-induced phosphorylations of the p70S6K1-S6 pathway and the expression of c-Fos. A reduction in c-Fos levels by dihydrocapsaicin led to a concomitant downregulation of AP-1 activation. Further analysis of the molecular mechanism responsible for the dihydrocapsaicin-mediated decrease in phospho-p70S6K1, revealed that dihydrocapsaicin can block amino acid-dependent mechanistic targets of rapamycin complex 1 (mTORC1)-p70S6K1-S6 signal activation. Additionally, dihydrocapsaicin was able to selectively augment amino acid deprivation-induced cell death in mTORC1-hyperactive cells. Collectively, dihydrocapsaicin exerted chemopreventive effects through inhibiting amino acid signaling and c-Fos pathways and, thus, might be a promising cancer preventive natural agent.


Dihydrocapsaicin Inhibits Epithelial Cell Transformation Through Targeting Amino Acid Signaling and c-Fos Expression


Ji Su Lee 1 , Yeong A Kim 2 3 , Young Jin Jang 4 , Yongtaek Oh 5 , Sanguine Byun 6

Publish date

2019 Jun 4




Cardiac arrest (CA) is one of the leading causes of mortality and morbidity in the world. Fast, reversible and controllable pharmaceutical-induced hypothermia (PIH) is strongly desired to treat ischemia-reperfusion brain injury. Dihydrocapsaicin (DHC), an agonist of transient receptor potential vanilloid type 1 cation channel (TRPV1), is an emerging candidate for PIH. Its capability to lower body temperature has been validated in both healthy and stroke animal models. However, DHC has shown cardiovascular effects and its safety and feasibility in a CA model has not been tested. Additionally, activated TRPV1 has multiple functions in addition to regulating body temperature and its effect on neurological recovery needs to be evaluated. In this study, we compared two methods of DHC administration, bolus injection and infusion via the femoral vein. We found that cardiovascular effects were only seen with a large dose DHC bolus injection. Then, we applied DHC-induced hypothermia in an asphyxial-CA rat model. We showed that DHC-treated rats were viable. Four-hour infusion of DHC at a rate of 0.75 mg/kg/h after CA maintained a body temperature of about 34 °C for at least 8 hours. DHC-treated rats had higher electrical activity during the first 4 hours after CA and had better neurological recovery during the 3 days after CA compared with normothermia rats. Additional pathway investigation of DHC administration following CA will further uncover the benefits of DHC-induced hypothermia.


Dihydrocapsaicin-induced Hypothermia After Asphyxiai Cardiac Arrest in Rats


Junyun He, Leanne Young, Xiaofeng Jia

Publish date

2016 Aug

Description :

Dihydrocapsaicin is a natural capsaicin, acts as a selective TRPV1 agonist, and also increases p-Akt levels. Dihydrocapsaicin enhances the hypothermia-induced neuroprotection[1][2].