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    Oroxylin A
    CAS No. 480-11-5 Price $138 / 20mg
    Catalog No.CFN98540Purity>=98%
    Molecular Weight284.26Type of CompoundFlavonoids
    FormulaC16H12O5Physical DescriptionYellow powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Oroxylin A Description
    Source: The seeds of Oraxylum indicum (L.) Kurz
    Biological Activity or Inhibitors: 1. Oroxylin A has anti-inflammation activity, it can inhibit LPS-induced iNOS and COX-2 gene expression by blocking NF-κB activation.
    2. Oroxylin A has selective antitumor effects, it preferentially inhibits the viability of hepatocellular carcinoma (HCC) cell line HepG2 but not the normal hepatic cell line L02.
    3. Oroxylin A reverses MDR by G2/M arrest and the underlying mechanism attributed to the suppression of P-gp expression via Chk2/P53/NF-κB signaling pathway.
    4. Oroxylin A suppresses invasion through down-regulating the expression of matrix metalloproteinase-2/9 in MDA-MB-435 human breast cancer cells, it may be developed as a therapeutic potential candidate for the treatment of cancer metastasis.
    5. Baicalin and its metabolites, baicalein and oroxylin A has anti-pruritic effect, oral baicalin may be metabolized by intestinal microflora into baicalein and oroxylin A, which ameliorate pruritic reactions through anti-histamine action.
    6. Oroxylin A has antithrombotic activities in vitro and in vivo.
    7. Oroxylin A facilitates memory consolidation through brain-derived neurotrophic factor (BDNF)-TrkB signaling and confirms that the increase of BDNF in a specific time window plays a crucial role in memory consolidation.
    8. Oroxylin A has antibacterial activity against a panel of susceptible and resistant Gram-positive and Gram-negative organisms.
    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.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

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    doi: 10.1016/j.molcel.2017.10.022.

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.5179 mL 17.5895 mL 35.1791 mL 70.3581 mL 87.9477 mL
    5 mM 0.7036 mL 3.5179 mL 7.0358 mL 14.0716 mL 17.5895 mL
    10 mM 0.3518 mL 1.759 mL 3.5179 mL 7.0358 mL 8.7948 mL
    50 mM 0.0704 mL 0.3518 mL 0.7036 mL 1.4072 mL 1.759 mL
    100 mM 0.0352 mL 0.1759 mL 0.3518 mL 0.7036 mL 0.8795 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.
    Oroxylin A References Information
    Citation [1]

    Brain Res Bull. 2014 Sep;108:67-73.

    Oroxylin A enhances memory consolidation through the brain-derived neurotrophic factor in mice.[Pubmed: 25218897]
    Memory consolidation is a process by which acquired information is transformed from a labile into a more stable state that can be retrieved at a later time. In the present study, we investigated the role of Oroxylin A on the memory consolidation process in mice. Oroxylin A improved the memory retention administered at 0 h, 1 h and 3 h after training in a passive avoidance task, suggesting that Oroxylin A facilitates memory consolidation. Oroxylin A increased mature brain-derived neurotrophic factor (mBDNF) levels in the hippocampus from 6h to 24h after administration. Moreover, 3h post-training administration of Oroxylin A enhanced the mBDNF level at 9h after the acquisition trial compared to the level at 6h after the acquisition trial. However, 6h post-training administration of Oroxylin A did not increase the mBDNF level at 9h after the acquisition trial. Blocking mBDNF signaling with recombinant tropomyosin receptor kinase B (TrkB)-Fc or k252a at 9h after the acquisition trial obstructed the effect of Oroxylin A on memory consolidation. Taken together, our data suggest that Oroxylin A facilitates memory consolidation through BDNF-TrkB signaling and confirms that the increase of BDNF in a specific time window plays a crucial role in memory consolidation.
    Citation [2]

    Arch Pharm Res. 2014 May;37(5):679-86.

    Antithrombotic activities of oroxylin A in vitro and in vivo.[Pubmed: 23963976]
    Here, the anticoagulant activities of Oroxylin A (OroA), a major component of Scutellaria baicalensis Georgi, were examined by monitoring activated partial thromboplastin time (aPTT), prothrombin time (PT), and the activities of cell-based thrombin and activated factor X (FXa). Furthermore, the effects of OroA on the expressions of plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (t-PA) were tested in tumor necrosis factor (TNF)-α activated human umbilical vein endothelial cells (HUVECs). Treatment with OroA resulted in prolonged aPTT and PT and inhibition of the activities of thrombin and FXa, and OroA inhibited production of thrombin and FXa in HUVECs. And OroA inhibited thrombin-catalyzed fibrin polymerization and platelet aggregation. In accordance with these anticoagulant activities, OroA elicited anticoagulant effects in mouse. In addition, treatment of OroA resulted in the inhibition of TNF-α-induced production of PAI-1, and treatment with OroA resulted in the significant reduction of the PAI-1 to t-PA ratio. Collectively, OroA possess antithrombotic activities and offer bases for development of a novel anticoagulant.
    Citation [3]

    Acta Pharmacol Sin. 2010 Jun;31(6):718-24.

    Anti-pruritic effect of baicalin and its metabolites, baicalein and oroxylin A, in mice.[Pubmed: 20453872 ]
    Baicalin was metabolized to baicalein and Oroxylin A, with metabolic activities of 40.2+/-26.2 and 1.2+/-1.1 nmol.h(-1).mg(-1) wet weight of human fecal microflora, respectively. Baicalin (20, 50 mg/kg) showed more potent inhibitory effect on histamine-induced scratching behavior when orally administered than intraperitoneally. In contrast, baicalein and Oroxylin A had more potent inhibitory effect when the intraperitoneally administered. The anti-scratching behavior activity of oral baicalin and its metabolites was in proportion to their inhibition on histamine-induced increase of vascular permeability with Oroxylin A more potent than baicalein and baicalin. In Magnus test using guinea pig ileum, Oroxylin A is more potent than baicalein and baicalin in inhibition of histamine-induced contraction. The anti-scratching behavioral effect of oral baicalin was significantly reduced when oral antibiotics were simultaneously administered, whereas the effect of baicalein and Oroxylin A were not affected. CONCLUSION: Oral baicalin may be metabolized by intestinal microflora into baicalein and Oroxylin A, which ameliorate pruritic reactions through anti-histamine action.
    Citation [4]

    Eur. J. Pharmacol., 2009, 603(1-3):22-8.

    Oroxylin A suppresses invasion through down-regulating the expression of matrix metalloproteinase-2/9 in MDA-MB-435 human breast cancer cells.[Pubmed: 19100732]
    Our previous study revealed that Oroxylin A, a naturally occurring monoflavonoid isolated from Scutellariae radix, could inhibit the proliferation of human hepatocellular carcinoma HepG2 cells through inducing the apoptosis in these cells. However, the molecular mechanism of its anticancer activity remains poorly understood and warrants further investigations. In this study, we examined the anti-invasive activities of Oroxylin A in vitro. The results showed that Oroxylin A suppressed MDA-MB-435 cell adhesion to the fibronectin-coated substrate in a concentration-dependent manner. It inhibited the wound healing migration of MDA-MB-435 cells and invasion of MDA-MB-435 cells through reconstituted extracellular matrix (matrigel). Zymography revealed that Oroxylin A decreased the secretion of matrix metalloproteinases-2 (MMP-2) and metalloproteinases-9 (MMP-9). Oroxylin A also inhibited the expressions of MMP-2 and MMP-9 in MDA-MB-435 cells. Additionally, Oroxylin A exerted an inhibitory effect on the phosphorylation of extracellular regulated proteinkinases1/2 (ERK1/2). Collectively, these data provided a molecular basis for the antiinvasive effects of Oroxylin A. Taken together, these findings strongly suggest that Oroxylin A had potential anti-metastatic effect in vitro and shed light on the investigation of Oroxylin A on breast cancer metastasis in vivo.
    Citation [5]

    Toxicol Lett. 2013 May 23;219(2):107-15.

    Oroxylin A reverses P-glycoprotein-mediated multidrug resistance of MCF7/ADR cells by G2/M arrest.[Pubmed: 23470866]
    Oroxylin A is a naturally occurring monoflavonoid isolated from the root of Scutellaria baicalensis Georgi, which has been used in traditional Chinese medicine for its anti-tumor, anti-inflammatory and anti-bacterial properties. The purpose of this study is to investigate the reversal effect and the fundamental mechanisms of Oroxylin A in MCF7/ADR cells. Data indicated that Oroxylin A showed strong reversal potency in MCF7/ADR cells and the reversal fold (RF) reached 4.68. After treatment with Oroxylin A, MCF7/ADR cells displayed reduced functional activity and expression of MDR1 at both the protein and mRNA levels. Meanwhile, Oroxylin A induced cells G2/M arrest in a concentration-dependent manner by increasing the expression of p-Chk2 (Thr68). Moreover, western blot and EMSA assays were used to reveal the inhibition of NF-κB in nucleus and the suppression of NF-κB binding activity by Oroxylin A. NSC 109555 ditosylate-Chk2 inhibitor partly dismissed G2/M arrest induced by Oroxylin A, reversed the increased trend of p-Chk2 and p-P53 (Ser20), inhibited the decreasing effect of Oroxylin A on the expression of P-gp and decreased the reversal fold of 90 μM Oroxylin A from 4.68 fold to 1.73 fold. In conclusion, we suggested that Oroxylin A reversed MDR by G2/M arrest and the underlying mechanism attributed to the suppression of P-gp expression via Chk2/P53/NF-κB signaling pathway.
    Citation [6]

    Toxicol Lett. 2012 Jul 20;212(2):113-25.

    Activation of the unfolded protein response contributed to the selective cytotoxicity of oroxylin A in human hepatocellular carcinoma HepG2 cells.[Pubmed: 22609744 ]
    Hepatocellular carcinoma (HCC) is a refractory malignancy with a high incidence and large mortality. Current strategy for the chemotherapy of HCC focuses on developing agents with better efficacy and lower toxicity. In this study, we demonstrated that the natural flavonoid Oroxylin A preferentially inhibited the viability of HCC cell line HepG2 but not the normal hepatic cell line L02. In HepG2 but not L02 cells, Oroxylin A induced substantial production of intracellular H₂O₂ and inordinate activation of the PERK-eIF2α-ATF4-CHOP branch of the unfolded protein response (UPR) pathway, which resulted in the induction of TRB3 and causal reduction of p-AKT1/2/3 (Ser473). Moreover, these effects were eliminated by either the stable knockdown of CHOP or the pretreatment and then co-incubation with the specific H₂O₂ scavenger catalase. These results indicated that the H₂O₂-triggered overactivation of the UPR pathway and causal inactivation of AKT signaling contributed to the preferential cytotoxicity of Oroxylin A in malignant HepG2 cells. Therefore, present study proposed an underlying molecular mechanism that implicated the selective antitumor effect of Oroxylin A and recommended Oroxylin A as a prospect for improving the current chemotherapeutic strategy for the treatment of HCC.
    Citation [7]

    Bioorg Med Chem Lett. 2005 Sep 1;15(17):3953-6.

    Synthesis and in vitro study of novel 7-O-acyl derivatives of Oroxylin A as antibacterial agents.[Pubmed: 16046127 ]
    A series of Oroxylin A derivatives, prepared by alkylation and condensation, were fully characterized by spectroscopic methods. All the derivatives were screened for antibacterial activity against a panel of susceptible and resistant Gram-positive and Gram-negative organisms. It was observed that acylation of 7-OH group in Oroxylin A significantly enhanced the activity as compared to their parent compound (Oroxylin A).
    Citation [8]

    Biochem Pharmacol. 2000 Jun 1;59(11):1445-57.

    Oroxylin A inhibition of lipopolysaccharide-induced iNOS and COX-2 gene expression via suppression of nuclear factor-kappaB activation.[Pubmed: 10751555]
    The results indicated that only Oroxylin A and emodin concentration-dependently inhibited LPS-induced NO production. The remaining compounds slightly inhibited LPS-induced NO production only at the highest concentration examined. Furthermore, Oroxylin A inhibited the expression of LPS-induced iNOS and COX-2 proteins and mRNAs without an appreciable cytotoxic effect on RAW264.7 cells. Emodin also inhibited LPS-induced iNOS protein as potently as Oroxylin A, but it inhibited LPS-induced iNOS mRNA expression only slightly and did not affect COX-2 mRNA and proteins. This was consistent with the findings that Oroxylin A but not emodin or physcion inhibited prostaglandin E(2) synthesis induced by LPS. The inhibitory effects of Oroxylin A on LPS-induced iNOS and COX-2 gene expression were also demonstrated in Bcl-2-overexpressing RAW264.7 macrophages, suggesting that Oroxylin A inhibition of iNOS and COX-2 expression was not due to its antioxidant effect. Furthermore, Oroxylin A but not emodin blocked nuclear factor-kappaB (NF-kappaB) binding and transcriptional activation associated with decreased p65 proteins in the nucleus induced by LPS. These results indicated that Oroxylin A, an active component in Huang Qin, inhibited LPS-induced iNOS and COX-2 gene expression by blocking NF-kappaB activation, whereas emodin inhibition of LPS-induced iNOS expression may be mediated by a different transcription factor.