We Offer Worldwide Shipping
Login Wishlist



  • Brand : BIOFRON

  • Catalogue Number : AV-P12342

  • Specification : 98%

  • CAS number : 6066-49-5

  • Formula : C12H14O2

  • Molecular Weight : 190.24

  • PUBCHEM ID : 61361

  • Volume : 50mg

Available on backorder

Checkout Bulk Order?

Catalogue Number


Analysis Method






Molecular Weight



Colorless oily matter

Botanical Source

Structure Type



Standards;Natural Pytochemical;API




3-Butyl-phthalide/1(3H)-Isobenzofuranone, 3-butyl-/3-Butyl-2-benzofuran-1(3H)-one/Butylphthalide/3-n-butylphthalide/3-Butylphthalide




1.1±0.1 g/cm3


Methanol; Chloroform

Flash Point

128.3±22.2 °C

Boiling Point

312.8±31.0 °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#:6066-49-5) 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.




Experimental animal study of treatment of Spinal cord injury (SCI).

This report aims to evaluate the in vivo effects of Butylphthalide NBP) on SCI biology and to explore its potential mechanism.

Spinal cord injury (SCI) causes great damage to humans. The inflammatory and reconstructive processes after SCI is regulated by activation of astroglial and microglial cells. Activated microglia/macrophages can be divided into M2 (anti-inflammatory) and M1 (pro-inflammatory) phenotypes. Butylphthalide (3-n-butylphthalide or NBP) treatment can significantly alleviate ischemic brain damage, and further study has confirmed that central neuroprotective effects can be realized by converting M1 polarized microglia/macrophages to the M2 phenotype. Thus far, it remains unknown whether NBP can modulate the transition of macrophages/microglia between the M1 and M2 phenotypes.

We randomly divided male mice into three groups (sham group, SCI group, SCI+ NBP group). Molecular and histological tests were performed to detect the macrophage/microglia polarization as well as the potential mechanism of NBP in vivo and in vitro.

It was found that NBP treatment significantly attenuated the motor dysfunction and neuronal apoptosis induced by SCI. Treatment with NBP could also reduce pro-inflammatory cytokine release after SCI and could facilitate macrophage/microglia M2 polarization and inhibit M1 polarization after SCI. To verify the findings in animal experiments, we examined the effect of NBP on BV2 cell polarization, the results showed that NBP treatment could enhance M2 polarization and inhibit M1 polarization, and that M2 polarization occurred in a p38-dependent manner.

NBP plays an important role in the anti-inflammatory response in SCI via the facilitation of macrophage/microglia M2 polarization as well as the inhibition of macrophage/microglia M1 polarization. The M2 polarization of macrophages/microglia occurs via activation of p38 pathway.



Butylphthalide has an Anti-Inflammatory Role in Spinal Cord Injury by Promoting Macrophage/Microglia M2 Polarization via p38 Phosphorylation.


Wang L1,2, He XJ1.

Publish date

2020 Mar 19




To investigate the alteration in Golgi and blood-brain barrier after cerebral hemorrhage in SD rats, and to evaluate the effect of butylphthalide on blood-brain barrier. ? Methods: Sprague-Dawley rats were randomly distributed into 4 groups: a control group, a sham group, an intracerebral hemorrhage (ICH) group, and a butylphthalide group. Brain tissue was collected at 48 h after the blood brain barrier permeability was examined. Western blotting and real-time polymerase chain reaction (real-time PCR) were conducted to explore the change of GM130, Cdc42 and tight junction protein and mRNA expression in rat brain after ICH. Immunohistochemistry (IHC) was performed to explore the distribution of ZO-1 and Occludin in the cerebral vascular endothelial cells around the hematoma.? Results: The Evans blue (EB) extravasation in the ICH group were much greater than that in the sham group (P<0.05). Butylphthalide treatment significantly decreased Evans blue extravasation compared to the ICH group (P<0.05). Results of Western blotting and real-time PCR showed that GM130, Cdc42, ZO-1/Occludin were decreased (P<0.05). The intervention of butylphthalide significantly upregulated the expressions of Cdc42 as well as ZO-1/Occludin (P<0.05), but exerted no effect on GM130 (P<0.05). Immunofluorescent staining showed that GM130 was co-localized with Cdc42 and administration of butylphthalide improved the expression of Cdc42 around the hematoma without affecting the expression of GM130. IHC showed that expressions of occludin and ZO-1 around the hematoma were significantly decreased in the ICH group (P<0.05), whereas butylphthalide treatment elevated the expressions of ZO-1 and occludin around the hematoma compared with the ICH group (P<0.05).? Conclusion: Morphology of Golgi apparatus is altered and the blood-brain barrier is destroyed after ICH. The application of butylphthalide can alleviate neurological impairment and blood-brain barrier disruption, which is related to the up-regulation of Cdc42, but not GM130.


[Effect of butylphthalide on blood-brain barrier after cerebral hemorrhage in SD rats and the mechanisms].


Qiu K1, Deng S1, Liu H1, You H2, Lei Q1, Lu W1.

Publish date

2019 Dec 28




Background and Objective: Transient ischemic attack (TIA) is a serious condition that is often called a warning stroke. The risk of cerebral infarction in patients with TIA and positive DWI findings is greater than that in patients with TIA and normal DWI findings. Butylphthalide injection is a new type of brain protective drug. The study aimed to determine the efficacy and safety of butylphthalide injection for treating TIA as shown by DWI abnormality progressing to infarction.Methods: We studied 98 patients with positive DWI findings among 260 patients with TIA, and randomly divided into the experimental (treatment with butylphthalide injection) and control (treatment with aspirin) groups. The number of cerebral infarctions in the two groups was recorded on 7th, 14th, 30th and 90th day, and adverse reactions were observed. The number of cerebral infarctions was compared among the different ABCD2 scores of patients with TIA and positive DWI findings.Results: The incidence of cerebral infarction in the experimental group was significantly lower than that in the control group (p < .05). The incidence of cerebral infarction with an ABCD2 score less than 3 points was significantly lower than that with an ABCD2 score of more than 3 points (p < .05), with less adverse reactions.Conclusion: Butylphthalide injection is helpful and safe for preventing stroke following TIA, and treating TIA with positive DWI and progression to infarction.


Transient ischemic attack; butylphthalide injection; cerebral infarction; diffusion-weighted magnetic resonance imaging; lesion


Effects of butylphthalide injection on treatment of transient ischemic attack as shown by diffusion-weighted magnetic resonance imaging abnormality.


Zhang C1, Zang Y2, Song Q3, Zhao W3, Li H1, Hu L1, Zhang Q1, Gu F4, Zhang C1.

Publish date

2020 Jan 14

Description :

Butylphthalide(3-n-Butylphthalide) is an anti-cerebral-ischemia drug; first isolated from the seeds of celery, showed efficacy in animal models of stroke.IC50 value:Target:3-n-butylphthalide alleviates oxidative stress caused by chronic cerebral ischemia, improves cholinergic function, and inhibits amyloid beta accumulation, thereby improving cerebral neuronal injury and cognitive deficits [2]. Intragastric NBP administration to 4-month-old SAMP8 mice for 2 months significantly improved spatial learning and memory ability. Moreover, the loss of choline acetyltransferase (ChAT)-positive neurons in the medial septal nucleus and the vertical limb of the diagonal band in SAMP8 mice was slowed down, as was the decline in the protein and mRNA expression of ChAT in the hippocampus, cerebral cortex, and forebrain [4].