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    Catalog No. CFN90235 Purity >=98% Price $188 / 20mg
    M. F C12H14O2 M. W 190.24
    Physical Description Oil Type of Compound Miscellaneous
    Identify | Grade NMR | HPLC Certification ChemFaces was verified by ISO2008:9001 certificate
    Chemical Structure 3-n-Butylphthalide
    Chemical Information Download 3-n-Butylphthalide-SDF
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  • 3-n-Butylphthalide Description
    Source: The herbs of Ligusticum jeholense
    Biological Activity
    or Inhibitors:
    1. Dl-3-n-Butylphthalide has antihypertensive effects, may slow the progression of hypertensive nephropathy by a variety of mechanisms.
    2. 3-n-Butylphthalide is effective for improving cognitive and global functioning in patients with subcortical VCIND and exhibits good safety, this effect might be mediated by preventing the decline of the central cholinergic system.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 5.2565 mL 26.2826 mL 52.5652 mL 105.1304 mL 131.413 mL
    5 mM 1.0513 mL 5.2565 mL 10.513 mL 21.0261 mL 26.2826 mL
    10 mM 0.5257 mL 2.6283 mL 5.2565 mL 10.513 mL 13.1413 mL
    50 mM 0.1051 mL 0.5257 mL 1.0513 mL 2.1026 mL 2.6283 mL
    100 mM 0.0526 mL 0.2628 mL 0.5257 mL 1.0513 mL 1.3141 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better
                 solubility within lower of Concentrations.
    3-n-Butylphthalide References Information
    Citation [1]

    Alzheimers Dement. 2015 Jun 15.

    The effects of DL-3-n-butylphthalide in patients with vascular cognitive impairment no dementia caused by subcortical ischemic small vessel disease: A multicentre, randomized, double-blind, placebo-controlled trial.[Pubmed: 26086183]
    Preclinical trials showed that dl-3-n-Butylphthalide (NBP) is effective for cognitive impairment of vascular origin. Patients were randomly assigned to dl-3-n-Butylphthalide 200 mg three times daily or matched placebo (1:1) for 24 weeks according to a computer-generated randomization protocol. RESULTS: This study enrolled 281 patients. dl-3-n-Butylphthalide showed greater effects than placebo on ADAS-cog (dl-3-n-Butylphthalide change -2.46 vs. placebo -1.39; P = .03; ITT) and CIBIC-plus (80 [57.1%] vs. 59 [42.1%] patients improved; P = .01; ITT). dl-3-n-Butylphthalide-related AE were uncommon and primarily consisted of mild gastrointestinal symptoms. CONCLUSIONS: Over the 6-month treatment period, dl-3-n-Butylphthalide was effective for improving cognitive and global functioning in patients with subcortical VCIND and exhibited good safety.
    Citation [2]

    Acta Pharmacol Sin. 2015 Jun 15.

    The edaravone and 3-n-butylphthalide ring-opening derivative 10b effectively attenuates cerebral ischemia injury in rats.[Pubmed: 26073328]
    AIM: Compound 10b is a hybrid molecule of edaravone and a ring-opening derivative of 3-n-Butylphthalide (NBP). The aim of this study was to examine the effects of compound 10b on brain damage in rats after focal cerebral ischemia. METHODS: SD rats were subjected to 2-h-middle cerebral artery occlusion (MCAO). At the onset of reperfusion, the rats were orally treated with 3-n-Butylphthalide (60 mg/kg), edaravone (3 mg/kg), 3-n-Butylphthalide (60 mg/kg)+edaravone (3 mg/kg), or compound 10b (70, 140 mg/kg). The neuroprotective effects of compound 10b were more pronounced compared to 3-n-Butylphthalide, edaravone or 3-n-Butylphthalide+edaravone. Furthermore, compound 10b significantly upregulated the protein levels of the cytoprotective molecules Bcl-2, HO-1, Nrf2, Trx, P-NF-κB p65, and IκB-α, while decreasing the expression of Bax, caspase 3, caspase 9, Txnip, NF-κB p65, and P-IκB-α. CONCLUSION: Oral administration of compound 10b effectively attenuates rat cerebral ischemia injury.
    Citation [3]

    Mol Med Rep. 2015 Feb;11(2):1448-54.

    Protective effect of 3-n-butylphthalide against hypertensive nephropathy in spontaneously hypertensive rats.[Pubmed: 25352064]
    Previous studies have demonstrated that a natural product of celery seeds, 3-n-Butylphthalide (NBP), has significant antihypertensive effects that are widely utilized in Chinese traditional medicine. The present study aimed to investigate the effects of 3-n-Butylphthalide on hypertensive nephropathy, as well as the mechanisms underlying this disease in spontaneously hypertensive rats (SHRs). SHRs were treated orally with saline, 3-n-Butylphthalide (15 or 30 mg/kg) or losartan (10 mg/kg) daily for 20 weeks, during which time blood pressure was measured every four weeks.The results showed that 3-n-Butylphthalide effectively attenuated progression of hypertensive nephropathy by decreasing urinary albumin excretion and blood urea nitrogen levels. It significantly decreased blood pressure (although less markedly than losartan) and the incidence of glomerulosclerosis. In addition, it alleviated tubular impairment and significantly decreased oxidative stress, as well as the expression of pro‑inflammatory cytokines and TGF-‑β1 in kidney tissues. In conclusion, the results suggested that 3-n-Butylphthalide may slow the progression of hypertensive nephropathy by a variety of mechanisms.
    Citation [4]

    Drug Metab Dispos. 2014 Apr;42(4):774-81.

    Bioactivation of 3-n-butylphthalide via sulfation of its major metabolite 3-hydroxy-NBP: mediated mainly by sulfotransferase 1A1.[Pubmed: 24468743]
    3-n-Butylphthalide (NBP) [(±)-3-butyl-1(3H)-isobenzofuranone] is an anti-cerebral-ischemia drug. Moderate hepatotoxicity has been observed in clinical applications. One of the major metabolites, 3-N-acetylcysteine-3-n-Butylphthalide, has been detected in human urine, indicating the formation of a reactive metabolite. We elucidated the formation mechanism of the reactive metabolite and its association with the hepatotoxicity of 3-n-Butylphthalide. The in vitro incubations revealed that 3-glutathione-3-n-Butylphthalide (3-GSH-NBP) was observed only in fresh rat liver homogenate rather than in liver microsomes, liver cytosol, or liver 9,000g supernatant supplemented with NADPH and GSH. We also detected 3-GSH-3-n-Butylphthalide when 3'-phosphoadenosine-5'-phosphosulfate was added in GSH-fortified human liver cytosol (HLC). The formation of 3-GSH-3-n-Butylphthalide was 39.3-fold higher using 3-hydroxy-3-n-Butylphthalide (3-OH-NBP) as the substrate than 3-n-Butylphthalide. The sulfotransferase (SULT) inhibitors DCNP (2,6-dichloro-4-nitrophenol) and quercetin suppressed 3-GSH-3-n-Butylphthalide formation in HLC by 75 and 82%, respectively, suggesting that 3-OH-NBP sulfation was involved in 3-GSH-3-n-Butylphthalide formation. Further SULT phenotyping revealed that SULT1A1 is the major isoform responsible for the sulfation. Dose-dependent toxicity was observed in primary rat hepatocytes exposed to 3-OH-3-n-Butylphthalide, with an IC50 of approximately 168 μM. Addition of DCNP and quercetin significantly increased cell viability, whereas l-buthionine-sulfoximine (a GSH depleter) decreased cell viability. Overall, our study revealed the underlying mechanism for the bioactivation of NBP is as follows. 3-n-Butylphthalide is first oxidized to 3-OH-3-n-Butylphthalide and further undergoes sulfation to form 3-OH-3-n-Butylphthalide sulfate. The sulfate spontaneously cleaves off, generating highly reactive electrophilic cations, which can bind either to GSH to detoxify or to hepatocellular proteins to cause undesirable side effects.
    Citation [5]

    Neurol Res. 2014 Mar;36(3):224-33.

    Improvement of cognitive deficits in SAMP8 mice by 3-n-butylphthalide.[Pubmed: 24512016]
    The herbal extract 3-n-Butylphthalide (NBP) is used in clinical practice for ischemic patients in China. It has been shown to have various neuroprotective effects both in vitro and in vivo. In the present study, the effects of 3-n-Butylphthalide on learning and memory decline in the senescence-accelerated mouse prone-8 (SAMP8) animal model were investigated. Intragastric 3-n-Butylphthalide administration to 4-month-old SAMP8 mice for 2 months significantly improved spatial learning and memory ability.These results demonstrated that 3-n-Butylphthalide treatment starting at the age of 4 months protected from the learning/memory deficits with aging of SAMP8 mice, and that this effect might be mediated by preventing the decline of the central cholinergic system.