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  • Brand : BIOFRON

  • Catalogue Number : BF-P3003

  • Specification : 98%

  • CAS number : 481-42-5

  • Formula : C11H8O3

  • Molecular Weight : 188.17

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Ceratostigma minus,Plumbago zeylanica,Drosera peltata

Structure Type









DMSO : ≥ 150 mg/mL (797.11 mM)
H2O : < 0.1 mg/mL (insoluble)
*"≥" means soluble, but saturation unknown.

Flash Point

Boiling Point

Melting Point



InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

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For Reference Standard and R&D, Not for Human Use Directly.

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provides coniferyl ferulate(CAS#:481-42-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Plumbagin derived from the plant Plumbago indica, known as Chitrak in India, is an example of a medicinal compound used traditionally to cure a variety of ailments. Previous reports have indicated that it can inhibit the growth of Mycobacterium tuberculosis (Mtb), the causative agent of the deadly disease TB. In this investigation, we provide an insight into its mode of action. We show here that a significant mycobacterial target that is inhibited by plumbagin is the enzyme ThyX, a form of thymidylate synthase, that is responsible for the synthesis of dTMP from dUMP in various bacterial pathogens, including Mtb. Using a purified preparation of the recombinant version of Mtb ThyX, we demonstrate that plumbagin, a 2,4 napthoquinone, but not lawsone, a structurally related medicinal compound, inhibits its activity in vitro. We also show that the intracellular [dTTP]/[dATP] ratio in Mycobacterium smegmatis (Msm) cells decrease upon treatment with plumbagin, and this, in turn, leads to cell death. Such a conclusion is supported by the observation that over-expression of thyx in the plumbagin treated Msm cells leads to the restoration of viability. The results of our investigation indicate that plumbagin kills mycobacterial cells primarily by targeting ThyX, a vital enzyme required for their survival.


Mycobacterium tuberculosis thymidylate synthase (ThyX) is a target for plumbagin, a natural product with antimycobacterial activity


Apurba Sarkar 1, Shreya Ghosh 1, Rahul Shaw 1, Madhu Manti Patra 1, Fatema Calcuttawala 1, Noyonika Mukherjee 1, Sujoy K Das Gupta 1

Publish date

2020 Feb 4




Plumbagin, a natural naphthoquinone from the officinal leadwort, has recently been shown to exert promising anti-cancer effects. However, its therapeutic use is hampered by its failure to specifically reach tumors after intravenous administration, without secondary effects on normal tissues. Its poor solubility in water and rapid elimination following in vivo administration further limit its potential use. We hypothesize that the entrapment of plumbagin within PEGylated PLGA nanoparticles conjugated with transferrin, whose receptors are overexpressed on many types of cancer cells, could lead to a selective delivery of the drug to tumors following intravenous administration and enhance its chemotherapeutic effects. The objectives of this study were therefore to prepare and characterize transferrin-conjugated, PEGylated PLGA nanoparticles entrapping plumbagin, and to assess their anti-cancer efficacy in vitro as well as in tumor-bearing mice. The intravenous administration of transferrin-conjugated PEGylated PLGA nanoparticles resulted in the complete suppression of 10% of B16-F10 tumors and regression of 30% of the tumors, with improvement of the animal survival compared to controls. The treatment was well tolerated by the animals. Transferrin-bearing PEGylated PLGA nanoparticles entrapping plumbagin are therefore highly promising therapeutic systems, able to lead to tumor regression and even suppression after intravenous administration without visible toxicity.


Anti-Tumor Activity of Intravenously Administered Plumbagin Entrapped in Targeted Nanoparticles


Intouch Sakpakdeejaroen, Sukrut Somani, Partha Laskar, Craig Irving, Margaret Mullin, Christine Dufes

Publish date

2020 Jan 1;




Background: PLB is a natural naphthoquinone compound isolated from the roots of Plumbago indica plant. Our previous study reported the inhibitory effect of Plumbagin (PLB) on human endocrine resistant breast cancer cell growth and cell invasion.

Hypothesis/purpose: Since PLB is a naphthoquinone compound, it can be reduced by the cytosolic NADPH: quinone oxidoreductase 1 (NQO1) enzyme. NQO1 expression is upregulated in various types of aggressive cancer including breast cancer. This study investigated the impact of NQO1 on anti-cancer effects of PLB in endocrine-resistant breast cancer cells.

Study design: This study was an in vitro study using ER-positive cell line (MCF7) and endocrine-resistant cell lines (MCF7/LCC2 and MCF7/LCC9 cells).

Methods: The roles of NQO1 in anti-cancer activity of PLB were investigated by using NQO1 knockdown cells, NQO1 inhibitor and NQO1 overexpressed cells. To study the impact of NQO1 on the effects of PLB on cell viability, apoptosis, invasion and generation of ROS, the following assays were used: MTT assays, annexin V-PE/7-ADD staining flow cytometry, matrigel invasion assays and DCFHDA assays. To study the mechanism of how NQO1 mediated PLB effects in tamoxifen response and apoptosis, we assessed the levels of mRNA expression by using qRT-PCR.

Results: 1. In this study, NQO1 was upregulated in endocrine-resistant cells. 2. PLB did not change the expression of NQO1 but it was able to increase NQO1 activity. 3. The inhibitory effects of PLB on cell proliferation, cell invasion and expression of tamoxifen resistant gene were attenuated in NQO1 knockdown cells or in the presence of NQO1 inhibitor. 4. The effects of PLB to induce apoptosis and generate ROS were also decreased when NQO1 activity was inhibited or when the NQO1 expression was reduced. 5. The anti-cancer effects of PLB increased when NQO1 was upregulated.

Conclusion: The effects of PLB in endocrine-resistant breast cancer cells is dependent on NQO1’s activity.


Breast cancer; Endocrine resistance; Nqo1; Plumbagin.


NADPH: Quinone oxidoreductase 1 (NQO1) mediated anti-cancer effects of plumbagin in endocrine resistant MCF7 breast cancer cells


Nalinee Pradubyat 1, Nithidol Sakunrangsit 1, Apiwat Mutirangura 2, Wannarasmi Ketchart 3

Publish date

2020 Jan

Description :

Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases PUMID/DOI:25444924 Cancer Lett. 2015 Feb 1;357(1):265-78. Plumbagin, a vitamin K3 analog and a pro-oxidant, was employed and it induced apoptosis in both mouse and human T-cell lymphoma cell lines via increased oxidative stress, caspase activity and loss of mitochondrial membrane potential. The pro-oxidant and cytotoxic effects of Plumbagin were sensitive to antioxidants indicating a decisive role of cellular redox balance. Plumbagin induced persistent activation of JNK and pharmacological inhibition as well as shRNA-mediated JNK knock-down rescued cells from Plumbagin-induced apoptosis. Further, Plumbagin induced cytochrome c release, FasL expression and Bax levels via activation of JNK pathway. Exposure of lymphoma cells to Plumbagin led to inhibition of total and specific phosphatase activity, increased total protein S-glutathionylation and induced glutathionylation of dual specific phosphatase- 1 and 4 (MKP-1 and MKP-2). The in vivo anti-tumor efficacy of Plumbagin was demonstrated using a mouse model. In conclusion, oxidative stress mediated tumor cytotoxicity operates through sustained JNK activation via a novel redox-mediated regulation of MKP-1 and MKP-2. Plumbagin protects against glucocorticoid-induced osteoporosis through Nrf-2 pathway. PUMID/DOI:25939783 Cell Stress Chaperones. 2015 Jul;20(4):621-9. We studied the protective role of Plumbagin against GC-induced cell damage in MC3T3-E1 cells. The effect of dexamethasone (DEX) and Plumbagin on cell viability was determined. DEX showed as IC-50 value of 95 μM. Further, 10 μM Plumbagin treatment effectively ameliorated DEX-induced cell death by increasing the cell viability to 92 %. A further effect of Plumbagin on DEX-induced oxidative stress was determined through reactive oxygen species (ROS) level, lipid peroxide content, and antioxidant status. Plumbagin treatment significantly reversed the levels of oxidative stress and apoptotic markers and protected against DEX-induced cell damage. Further, Plumbagin treatment significantly improved the expression of osteogenic markers compared to DEX treatment. In conclusion, the present study shows that Plumbagin offers significant protective role against DEX-induced cellular damage via regulating oxidative stress, apoptosis, and osteogenic markers. Plumbagin induces growth inhibition of human glioma cells by downregulating the expression and activity of FOXM1. PUMID/DOI:25528634 J Neurooncol. 2015 Feb;121(3):469-77. Plumbagin, a natural quinonoid constituent isolated from the root of medicinal plant Plumbago zeylanica L, has exhibited anti-tumor and anti-proliferative activities in various tumor cell lines as well as in animal tumor models.We reported that Plumbagin could effectively inhibit cell proliferation, migration and invasion and induce apoptosis of glioma cells. Cell cycle assay showed that Plumbagin induced G2/M arrest. Interestingly, we found that Plumbagin decreased the expression of FOXM1 both at mRNA level and protein level. Plumbagin also inhibited the transactivation ability of FOXM1, resulting in down-regulating the expression of FOXM1 downstream target genes, such as cyclin D1, Cdc25B, survivin, and increasing the expression of p21(CIP1) and p27(KIP1). Most importantly, down-regulation of FOXM1 by siFOXM1 transfection enhanced Plumbagin-induced change in viability. On the contrary, over-expression of FOXM1 by cDNA transfection reduced Plumbagin-induced glioma cell growth inhibition. These results suggest that Plumbagin exhibits its anticancer activity partially by inactivation of FOXM1 signaling pathway in glioma cells. Our findings indicate that Plumbagin may be considered as a potential natural FOXM1 inhibitor, which could contribute to the development of new anticancer agent for therapy of gliomas. Anti-fibrotic effect of plumbagin on CCl₄-lesioned rats PUMID/DOI:25824458 Cell Physiol Biochem. 2015;35(4):1599-608. BACKGROUND/AIMS:||Our previous studies have shown that plumbagin effectively inhibits hepatic stellate cell (HSC) proliferation. Thus, plumbagin-mediated anti-fibrotic effects in vivo merit further investigation.||||METHODS:||We used rat models to assess the potential benefits of plumbagin against CCl?-induced liver fibrosis.||||RESULTS:||The results showed that plumbagin lowered the serum concentrations of liver functional enzymes (ALT, AST, ALB, TBIL) in CCl?-fibrotic rats while reducing inflammatory cytokine levels (IL-6, TNF-α). As reflected in pathological examinations, rats that were administered plumbagin showed decreased collagen markers (HA, LN, PCIII and CIV) in liver tissues and improved hepatocellular impairments. In addition, plumbagin contributed to down-regulating NF-κB and TLR-4 mRNA in CCl?-lesioned livers. As revealed in the immunohistochemical assay, plumbagin-administered rats showed reduced levels of α-SMA and TNF-α immunoreactive cells in liver tissue.||CONCLUSION:||Collectively, these findings offer appealing evidence that plumbagin may serve as an anti-fibrotic medication through inactivating the NF-κB/TLR-4 pathway that is associated with inflammatory reactions, thereby mitigating liver fibrosis. Plumbagin Nanoparticles Induce Dose and pH Dependent Toxicity on Prostate Cancer Cells. PUMID/DOI:25772029 Curr Drug Deliv. 2015 Mar 16. Stable nano-formulation of Plumbagin nanoparticles from Plumbago zeylanica root extract was explored as a potential natural drug against prostate cancer. Size and morphology analysis by DLS, SEM and AFM revealed the average size of nanoparticles prepared was 100±50nm. In vitro cytotoxicity showed concentration and time dependent toxicity on prostate cancer cells. However, Plumbagin crude extract found to be highly toxic to normal cells when compared to Plumbagin nanoformulation, thus confirming nano Plumbagin shows cytocompatibility with normal cells and dose dependent toxicity to prostate cells. In vitro haemolysis assay confirmed the blood biocompatibility of the Plumbagin nanoparticles. In wound healing assay, Plumbagin nanoparticles provided clues which might play an important role in the anti-migration of prostate cancer cells. DNA fragmentation revealed that partial apoptosis induction by Plumbagin nanoparticles could be expected as a potent anti-cancer agent against prostate cancer.