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  • Brand : BIOFRON

  • Catalogue Number : BN-O1406

  • Specification : 90%(HPLC)

  • CAS number : 116-26-7

  • Formula : C10H14O

  • Molecular Weight : 150.22

  • PUBCHEM ID : 61041

  • Volume : 0.1ml

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Catalogue Number


Analysis Method





Molecular Weight



Botanical Source

Structure Type





2,6,6-trimethylcyclohexa-1,3-dienecarbaldehyde/2,3-Dihydro-2,2,6-trimethylbenzaldehyde/Safranal/2,6,6-Trimethylcyclohexa-1,3-dienyl methanal/2,6,6-trimethyl-1,3-cyclohexadiene-1-carboxaldehyde/1,3-CYCLOHEXADIENE-1-CARBOXALDEHYDE,2,6,6-TRIMETHYL/2,6,6-trimethylcyclohexa-1,3-diene-1-carbaldehyde/1,1,3-Trimethyl-2-formylcyclohexa-2,4-diene




0.975 g/cm3


Flash Point


Boiling Point

217.3ºC 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#:116-26-7) 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.




The aim of the present study was to investigate the effects of safranal on cisplatin-induced nephrotoxicity and oxidative stress in rats. Adult male Sprague-Dawley rats were randomly divided into five groups. The control group received physiological saline; animals in Group 2 received only safranal and in Group 3 received only cisplatin; 5 days of safranal treatment was performed following administration of cisplatin for the animals in Group 4; 5 days of safranal pretreatment was applied to the animals in Group 5 before administration of cisplatin. Cisplatin (7 mg/kg) was intraperitoneally injected as a single dose and safranal (200 mg/kg) was administered by gavage. Biochemical and histopathological methods were utilized for evaluation of the nephrotoxicity. The concentrations of creatinine and urea in plasma and levels of malondialdehyde (MDA) and glutathione (GSH) as well as total antioxidant status (TAS) and total oxidant status (TOS) were determined in kidney tissue. Administration of cisplatin to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. MDA and TOS levels of rats that received cisplatin alone were not significantly different compared with those of the control group, but GSH and TAS levels in the only cisplatin-administered group were significantly decreased. Safranal administration produced amelioration in biochemical indices of nephrotoxicity in both plasma and kidney tissues when compared with the only cisplatin-administered group, pretreatment with safranal being more effective. As a result, safranal treatment might have a protective effect against cisplatin-induced nephrotoxicity and oxidative stress in rat.

© 2017 The Author(s); published by Portland Press Limited on behalf of the Biochemical Society.


antioxidants; cisplatin; histopathology; oxidative stress; safranal


Efficacy of safranal to cisplatin-induced nephrotoxicity.


Karafakıoglu YS1, Bozkurt MF2, Hazman o3, Fıdan AF4.

Publish date

2017 Mar 20




Safranal is one of saffron constituents and has antioxidant and neuroprotective properties. Metformin is used as an anti-diabetic drug. This study was planned to investigate the separate and combined treatment effects of safranal and metformin on diabetes-induced learning and memory impairments by behavioral and hippocampal histopathological and biochemical evaluations. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ), treatments with safranal (0.025, 0.1 and 0.4 mg/kg), metformin (50 and 200 mg/kg), and a combination of low doses of this chemicals were initiated after confirmation of diabetes and continued for 37 days. Blood glucose concentration was measured before and on days 15, 25 and 35 after injection of streptozotocin. Learning and memory tested using Morris Water Maze (MWM) on days 40-45 and on day 45 hippocampal specimens were collected for determination of malodialdehyde (MDA), tumor necrosis factor-alpha (TNF-α) and Caspase-3 levels and superoxide dismutase (SOD) activity. The hippocampus was also designed for light microscopy evaluation. Hyperglycemia, spatial learning and memory impairments, hippocampal neuron loss, increase of hippocampal MDA, TNF-α and caspase-3 levels and decrease of SOD activity were observed in diabetic rats. Safranal (0.1 and 0.4 mg/kg), metformin (200 mg/kg) and safranal (0.025 mg/kg) with metformin (50 mg/kg) improved the above-mentioned behavioral, histopathological and biochemical changes. Safranal and metformin and their combination improved learning and memory impairments in STZ-induced diabetic rats. Antioxidant, anti-inflammatory and antiapoptotic mechanisms might be involved. It is recommended that safranal be considered for diabetes management.

Copyright © 2018. Published by Elsevier Masson SAS.


Diabetes; Learning and memory impairments; Metformin; Rats; Safranal


The effects of safranal, a constitute of saffron, and metformin on spatial learning and memory impairments in type-1 diabetic rats: behavioral and hippocampal histopathological and biochemical evaluations.


Delkhosh-Kasmaie F1, Farshid AA2, Tamaddonfard E3, Imani M4.

Publish date

2018 Nov




Researches have been shown that glutamic acid (GA) or quinolinic acid (QA) can play role in neuroinflammatory and demyelinating diseases including multiple sclerosis (MS), mainly via oligodendrocytes activation and extreme free radicals generation. Recent studies have demonstrated that safranal, an active constituent of Crocus sativus, has several pharmacological effects such as antioxidant, anti-inflammatory and neuroprotective properties. Since there is no data about the impact of safranal on MS, this study was designed to investigate the protective effect of safranal on OLN-93 oligodendrocytes injury induced by GA or QA.

At first, the potential toxic effect of safranal on OLN-93 viability was evaluated. Also, the cells were pretreated with safranal (0.1, 1, 10, 50, 100 and 200 μM) for 2 h and then subjected to GA (16 mM) or QA (8 mM) toxicity for 24 h, in which the same treatments were applied. The cell viability and parameters of redox status such as the levels of intracellular reactive oxygen species (ROS) and lipid peroxidation were measured.

Safranal at concentration ranges of 1-800 μM had no toxic effect on cell viability (p>0.05). Treatment with safranal significantly increased cell viability following GA or QA insults at concentrations higher than 1 μM (p<0.01). The cytoprotective potential of safranal was also accompanied by decreased ROS accumulation (p<0.001) and malondialdehyde level (p<0.001) following GA or QA insults. CONCLUSION: The data suggests that safranal exhibits oligoprotection potential by means of inhibiting oxidative stress parameters. © Georg Thieme Verlag KG Stuttgart · New York.


Safranal Attenuates Excitotoxin-Induced Oxidative OLN-93 Cells Injury.


Alavi MS1,2, Fanoudi S3,2, Fard AV2, Soukhtanloo M4, Hosseini M3, Barzegar H2, Sadeghnia HR1,3,2.

Publish date

2019 Jun

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