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    3-n-Butylphthalide
    Information
    CAS No. 6066-49-5 Price $138 / 20mg
    Catalog No.CFN90235Purity>=98%
    Molecular Weight190.24Type of CompoundMiscellaneous
    FormulaC12H14O2Physical DescriptionOil
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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  • Biological Activity
    Description: Dl-3-n-Butylphthalide has antihypertensive effects, may slow the progression of hypertensive nephropathy by a variety of mechanisms.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.
    Targets: Bcl-2/Bax | Caspase | HO-1 | IkB | Nrf2 | p65 | NF-kB | TGF-β/Smad | IKK
    In vitro:
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    In vivo:
    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]
    Vascular cognitive impairment without dementia is very common among the aged and tends to progress to dementia, but there have been no proper large-scale intervention trials dedicated to it. Vascular cognitive impairment without dementia caused by subcortical ischemic small vessel disease (hereinafter, subcortical Vascular cognitive impairment without dementia) represents a relatively homogeneous disease process and is a suitable target for therapeutic trials investigating Vascular cognitive impairment without dementia. Preclinical trials showed that dl-3-n-Butylphthalide (NBP) is effective for cognitive impairment of vascular origin.
    METHODS AND RESULTS:
    In this randomized, double-blind, placebo-controlled trial, we enrolled patients aged 50-70 years who had a diagnosis of subcortical Vascular cognitive impairment without dementia at 15 academic medical centers in China. Inclusion criteria included a clinical dementia rating ≥0.5 on at least one domain and global score ≤0.5; a mini-mental state examination score ≥20 (primary school) or ≥24 (junior school or above); and brain magnetic resonance imaging consistent with subcortical ischemic small vessel disease. Patients were randomly assigned to NBP 200 mg three times daily or matched placebo (1:1) for 24 weeks according to a computer-generated randomization protocol. All patients and study personnel were masked to treatment assignment. Primary outcome measures were the changes in Alzheimer's disease assessment scale-cognitive subscale (ADAS-cog) and clinician's interview-based impression of change plus caregiver input (CIBIC-plus) after 24 weeks. All patients were monitored for adverse events (AEs). Outcome measures were analyzed for both the intention-to-treat (ITT) population and the per protocol population. This study enrolled 281 patients. NBP showed greater effects than placebo on ADAS-cog (NBP 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). NBP-related AE were uncommon and primarily consisted of mild gastrointestinal symptoms.
    CONCLUSIONS:
    Over the 6-month treatment period, NBP was effective for improving cognitive and global functioning in patients with subcortical vascular cognitive impairment without dementia and exhibited good safety.
    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]
    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 AND RESULTS:
    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.
    CONCLUSIONS:
    Oral administration of compound 10b effectively attenuates rat cerebral ischemia injury.
    3-n-Butylphthalide Description
    Source: The herbs of Ligusticum jeholense
    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).

    Wherever 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.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    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.
    Protocol
    Animal Research:
    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.
    METHODS AND RESULTS:
    The present study aimed to investigate the effects of NBP on hypertensive nephropathy, as well as the mechanisms underlying this disease in spontaneously hypertensive rats (SHRs). SHRs were treated orally with saline, NBP (15 or 30 mg/kg) or losartan (10 mg/kg) daily for 20 weeks, during which time blood pressure was measured every four weeks. At the end of the 20‑week treatment, blood and urine samples were collected for biochemical analysis, and kidney tissues were obtained for histopathological analysis and immunohistochemistry. Enzyme‑linked immunosorbent assays and western blotting were used to analyze the expression of transforming growth factor (TGF)‑β1 in blood and kidney tissues, respectively. The results showed that NBP 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.
    CONCLUSIONS:
    In conclusion, the results suggested that NBP may slow the progression of hypertensive nephropathy by a variety of mechanisms.
    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.
    METHODS AND RESULTS:
    In the present study, the effects of NBP on learning and memory decline in the senescence-accelerated mouse prone-8 (SAMP8) animal model were investigated. 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.
    CONCLUSIONS:
    These results demonstrated that NBP 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.