Beta-Lapachone

Beta-Lapachone
Product Name Beta-Lapachone
CAS No.: 4707-32-8
Catalog No.: CFN91668
Molecular Formula: C15H14O3
Molecular Weight: 242.27 g/mol
Purity: >=98%
Type of Compound: Quinones
Physical Desc.: Powder
Source: The barks of Catalpa ovata
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price:
Beta-Lapachone is a specific DNA topoisomerase I inhibitor, and induces apoptosis by inhibiting cell cycle progression, but no inhibitory activities against DNA topoisomerase II or ligase. Beta-lapachone can increase cell proliferation, including keratinocytes, fibroblasts, and endothelial cells, and migration of fibroblasts and endothelial cells and thus accelerate wound healing.
Inquire / Order: manager@chemfaces.com
Technical Inquiries: service@chemfaces.com
Tel: +86-27-84237783
Fax: +86-27-84254680

Address:
1 Building, No. 83, CheCheng Rd., Wuhan Economic and Technological Development Zone, Wuhan, Hubei 430056, PRC
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

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.
  • Mol Med Rep.2014, 9(5):1653-9
  • J Cell Mol Med.2023, 27(10):1423-1435.
  • Sci Rep.2019, 9:19059
  • Institut Pasteur Korea2020, doi: 10.21203.
  • J Chromatogr B Analyt Technol Biomed Life Sci.2018, 1080:27-36
  • Biol Pharm Bull.2018, 41(1):65-72
  • ACS Synth Biol.2022, 11(10):3296-3304.
  • Pharmacol Res.2020, 161:105205.
  • Int J Mol Sci.2018, 19(9):E2528
  • Org Biomol Chem.2017, 15(31):6483-6492
  • Dehydro-alpha-lapachone

    Catalog No: CFN99641
    CAS No: 15297-92-4
    Price: Inquiry(manager@chemfaces.com)
    alpha-Lapachone

    Catalog No: CFN98702
    CAS No: 4707-33-9
    Price: Inquiry(manager@chemfaces.com)
    9-Hydroxy-alpha-lapachone

    Catalog No: CFN98215
    CAS No: 22333-58-0
    Price: Inquiry(manager@chemfaces.com)
    9-Methoxy-alpha-lapachone

    Catalog No: CFN98463
    CAS No: 35241-80-6
    Price: Inquiry(manager@chemfaces.com)
    4,9-Dihydroxy-alpha-lapachone

    Catalog No: CFN98947
    CAS No: 56473-67-7
    Price: Inquiry(manager@chemfaces.com)
    Beta-Lapachone

    Catalog No: CFN91668
    CAS No: 4707-32-8
    Price: Inquiry(manager@chemfaces.com)
    J Biol Chem. 1993 Oct 25;268(30):22463-22468.
    beta-Lapachone, a novel DNA topoisomerase I inhibitor with a mode of action different from camptothecin[Pubmed: 8226754]
    Beta-Lapachone is a plant product that has been found to have many pharmacological effects. To date, very little is known about its biochemical target. In this study, we found that Beta-Lapachone inhibits the catalytic activity of topoisomerase I from calf thymus and human cells. But, unlike camptothecin, Beta-Lapachone does not stabilize the cleavable complex, indicating a different mechanism of action. Beta-Lapachone inhibits topoisomerase I-mediated DNA cleavage induced by camptothecin. Incubation of topoisomerase I with Beta-Lapachone before adding DNA substrate dramatically increases this inhibition. Incubation of topoisomerase I with DNA prior to Beta-Lapachone makes the enzyme refractory, and treatment of DNA with Beta-Lapachone before topoisomerase has no effect. These results suggest a direct interaction of Beta-Lapachone with topoisomerase I rather than DNA substrate. Beta-Lapachone does not inhibit binding of enzyme to DNA substrate. In cells, Beta-Lapachone itself does not induce a SDS-K(+)-precipitable complex, but it inhibits complex formation with camptothecin. We propose that the direct interaction of Beta-Lapachone with topoisomerase I does not affect the assembly of the enzyme-DNA complex but does inhibit the formation of cleavable complex.
    Mutat Res . 1998 Jun 5;401(1-2):55-63.
    DNA damage and cytotoxicity induced by beta-lapachone: relation to poly(ADP-ribose) polymerase inhibition[Pubmed: 9639674]
    Beta-Lapachone (3,4-dihydro-2,2-dimethyl-2H-naphtho[1,2-b]pyran-5, 6-dione) was previously shown to enhance the lethality of X-rays and radiomimetic agents and its radiosensitizing role in mammalian cells was attributed to a possible interference with topoisomerase I activity. Furthermore, Beta-Lapachone alone was found to induce chromosomal damage in Chinese hamster ovary (CHO) cells. The aim of the present study was to further elucidate the possible mechanisms by which Beta-Lapachone exerts its genotoxic action in cultured mammalian cells. Flow cytometry analysis of Beta-Lapachone-treated CHO cells indicated a selective cytotoxic effect upon S phase of the cell cycle. Beta-Lapachone produced DNA strand breaks as determined by alkaline elution assay; alkaline elution profiles from treated cells showed a bimodal dose-response pattern, with a threshold dose above which a massive dose-independent DNA degradation was observed. Furthermore, Beta-Lapachone increased the capacity of crude CHO cellular extracts to unwind supercoiled plasmid DNA, while significantly inhibiting in vitro poly(ADP-ribose) polymerase (PARP). These results suggest that damage induction is probably mediated by the interaction between Beta-Lapachone and cellular enzymatic function(s), rather than reflecting a direct action on the DNA. We suggest that the inhibition of PARP plays a central role in the complex biological effects induced by Beta-Lapachone in CHO cells.
    Cancer Res. 1995 Sep 1;55(17):3706-3711.
    Beta-lapachone-mediated apoptosis in human promyelocytic leukemia (HL-60) and human prostate cancer cells: a p53-independent response[Pubmed: 7641180]
    Beta-Lapachone and certain of its derivatives directly bind and inhibit topoisomerase I (Topo I) DNA unwinding activity and form DNA-Topo I complexes, which are not resolvable by SDS-K+ assays. We show that Beta-Lapachone can induce apoptosis in certain cells, such as in human promyelocytic leukemia (HL-60) and human prostate cancer (DU-145, PC-3, and LNCaP) cells, as also described by Li et al. (Cancer Res., 55: 0000-0000, 1995). Characteristic 180-200-bp oligonucleosome DNA laddering and fragmented DNA-containing apoptotic cells via flow cytometry and morphological examinations were observed in 4 h in HL-60 cells after a 4-h, > or = 0.5 microM Beta-Lapachone exposure. HL-60 cells treated with camptothecin or topotecan resulted in greater apoptotic DNA laddering and apoptotic cell populations than comparable equitoxic concentrations of Beta-Lapachone, although Beta-Lapachone was a more effective Topo I inhibitor. Beta-Lapachone treatment (4 h, 1-5 microM) resulted in a block at G0/G1, with decreases in S and G2/M phases and increases in apoptotic cell populations over time in HL-60 and three separate human prostate cancer (DU-145, PC-3, and LNCaP) cells. Similar treatments with topotecan or camptothecin (4 h, 1-5 microM) resulted in blockage of cells in S and apoptosis. Thus, Beta-Lapachone causes a block in G0/G1 of the cell cycle and induces apoptosis in cells before, or at early times during, DNA synthesis. These events are p53 independent, since PC-3 and HL-60 cells are null cells, LNCaP are wild-type, and DU-145 contain mutant p53, yet all undergo apoptosis after Beta-Lapachone treatment. Interestingly, Beta-Lapachone treatment of p53 wild type-containing prostate cancer cells (i.e., LNCaP) did not result in the induction of nuclear levels of p53 protein, as did camptothecin-treated cells. Like other Topo I inhibitors, Beta-Lapachone may induce apoptosis by locking Topo I onto DNA, blocking replication fork movement, and inducing apoptosis in a p53-independent fashion. Beta-Lapachone and its derivatives, as well as other Topo I inhibitors, have potential clinical utility alone against human leukemia and prostate cancers.
    Am J Physiol Cell Physiol. 2008 Oct;295(4):C931-943.
    In vitro and in vivo wound healing-promoting activities of beta-lapachone[Pubmed: 18650264]
    Impaired wound healing is a serious problem for diabetic patients. Wound healing is a complex process that requires the cooperation of many cell types, including keratinocytes, fibroblasts, endothelial cells, and macrophages. Beta-Lapachone, a natural compound extracted from the bark of the lapacho tree (Tabebuia avellanedae), is well known for its antitumor, antiinflammatory, and antineoplastic effects at different concentrations and conditions, but its effects on wound healing have not been studied. The purpose of the present study was to investigate the effects of Beta-Lapachone on wound healing and its underlying mechanism. In the present study, we demonstrated that a low dose of Beta-Lapachone enhanced the proliferation in several cells, facilitated the migration of mouse 3T3 fibroblasts and human endothelial EAhy926 cells through different MAPK signaling pathways, and accelerated scrape-wound healing in vitro. Application of ointment with or without Beta-Lapachone to a punched wound in normal and diabetic (db/db) mice showed that the healing process was faster in Beta-Lapachone-treated animals than in those treated with vehicle only. In addition, Beta-Lapachone induced macrophages to release VEGF and EGF, which are beneficial for growth of many cells. Our results showed that Beta-Lapachone can increase cell proliferation, including keratinocytes, fibroblasts, and endothelial cells, and migration of fibroblasts and endothelial cells and thus accelerate wound healing. Therefore, we suggest that Beta-Lapachone may have potential for therapeutic use for wound healing.
    Int J Tryptophan Res . 2013 Aug 19;6:35-45.
    The Tumor-Selective Cytotoxic Agent β-Lapachone is a Potent Inhibitor of IDO1[Pubmed: 24023520]
    β-lapachone is a naturally occurring 1,2-naphthoquinone-based compound that has been advanced into clinical trials based on its tumor-selective cytotoxic properties. Previously, we focused on the related 1,4-naphthoquinone pharmacophore as a basic core structure for developing a series of potent indoleamine 2,3-dioxygenase 1 (IDO1) enzyme inhibitors. In this study, we identified IDO1 inhibitory activity as a previously unrecognized attribute of the clinical candidate β-lapachone. Enzyme kinetics-based analysis of β-lapachone indicated an uncompetitive mode of inhibition, while computational modeling predicted binding within the IDO1 active site consistent with other naphthoquinone derivatives. Inhibition of IDO1 has previously been shown to breach the pathogenic tolerization that constrains the immune system from being able to mount an effective anti-tumor response. Thus, the finding that β-lapachone has IDO1 inhibitory activity adds a new dimension to its potential utility as an anti-cancer agent distinct from its cytotoxic properties, and suggests that a synergistic benefit can be achieved from its combined cytotoxic and immunologic effects.
    Pharmacol Rep . 2016 Feb;68(1):27-31.
    β-Lapachone enhances Mre11-Rad50-Nbs1 complex expression in cisplatin-induced nephrotoxicity[Pubmed: 26721347]
    Background: Recent studies suggest a potential involvement of the Mre11-Rad50-Nbs1 (MRN) complex, a DNA double-strand breaks (DSBs) sensor, in the development of nephrotoxicity following cisplatin administration. β-Lapachone is a topoisomerase I inhibitor known to reduce cisplatin-induced nephrotoxicity. In this study, by assessing MRN complex expression, we explored whether β-lapachone was involved in DNA damage response in the context of cisplatin-induced nephrotoxicity. Methods: Male Balb/c mice were randomly allocated to 4 groups: control, β-lapachone alone, cisplatin alone, and β-lapachone+cisplatin. β-Lapachone was administered with the diet (0.066%) for 2 weeks prior to cisplatin injection (18mg/kg). All mice were sacrificed 3 days after cisplatin treatment. Results: In the cisplatin-alone group, renal function was disrupted and MRN complex expression increased. As expected, β-lapachone co-treatment attenuated cisplatin-induced pathologic alterations. Notably, although β-lapachone markedly decreased cisplatin-induced renal cell apoptosis and DSBs formation, the β-lapachone+cisplatin group showed the highest MRN complex expression. Moreover, β-lapachone treatment increased the basal expression level of the MRN complex, which was accompanied by enhanced basal expression of SIRTuin1, which is known to regulate Nbs1 acetylation. Conclusion: Although, it remains unclear how β-lapachone induces MRN complex expression, our findings suggest that β-lapachone might affect MRN complex expression and participate in DNA damage recovery in cisplatin-induced nephrotoxicity.
    Am J Physiol Cell Physiol. 2008 Oct;295(4):C931-943.
    In vitro and in vivo wound healing-promoting activities of beta-lapachone[Pubmed: 18650264]
    Impaired wound healing is a serious problem for diabetic patients. Wound healing is a complex process that requires the cooperation of many cell types, including keratinocytes, fibroblasts, endothelial cells, and macrophages. Beta-Lapachone, a natural compound extracted from the bark of the lapacho tree (Tabebuia avellanedae), is well known for its antitumor, antiinflammatory, and antineoplastic effects at different concentrations and conditions, but its effects on wound healing have not been studied. The purpose of the present study was to investigate the effects of Beta-Lapachone on wound healing and its underlying mechanism. In the present study, we demonstrated that a low dose of Beta-Lapachone enhanced the proliferation in several cells, facilitated the migration of mouse 3T3 fibroblasts and human endothelial EAhy926 cells through different MAPK signaling pathways, and accelerated scrape-wound healing in vitro. Application of ointment with or without Beta-Lapachone to a punched wound in normal and diabetic (db/db) mice showed that the healing process was faster in Beta-Lapachone-treated animals than in those treated with vehicle only. In addition, Beta-Lapachone induced macrophages to release VEGF and EGF, which are beneficial for growth of many cells. Our results showed that Beta-Lapachone can increase cell proliferation, including keratinocytes, fibroblasts, and endothelial cells, and migration of fibroblasts and endothelial cells and thus accelerate wound healing. Therefore, we suggest that Beta-Lapachone may have potential for therapeutic use for wound healing.
    Proc Natl Acad Sci U S A . 1999 Nov 9;96(23):13369-13374.
    Potent inhibition of tumor survival in vivo by beta-lapachone plus taxol: combining drugs imposes different artificial checkpoints[Pubmed: 10557327]
    Ablation of tumor colonies was seen in a wide spectrum of human carcinoma cells in culture after treatment with the combination of Beta-Lapachone and taxol, two low molecular mass compounds. They synergistically induced death of cultured ovarian, breast, prostate, melanoma, lung, colon, and pancreatic cancer cells. This synergism is schedule dependent; namely, taxol must be added either simultaneously or after Beta-Lapachone. This combination therapy has unusually potent antitumor activity against human ovarian and prostate tumor prexenografted in mice. There is little host toxicity. Cells can commit to apoptosis at cell-cycle checkpoints, a mechanism that eliminates defective cells to ensure the integrity of the genome. We hypothesize that when cells are treated simultaneously with drugs activating more than one different cell-cycle checkpoint, the production of conflicting regulatory signaling molecules induces apoptosis in cancer cells. Beta-Lapachone causes cell-cycle delays in late G(1) and S phase, and taxol arrests cells at G(2)/M. Cells treated with both drugs were delayed at multiple checkpoints before committing to apoptosis. Our findings suggest an avenue for developing anticancer therapy by exploiting apoptosis-prone "collisions" at cell-cycle checkpoints.
    1,3,6-Tri-O-galloylglucose

    Catalog No: CFN95043
    CAS No: 18483-17-5
    Price: $318/10mg
    5,7,2',4'-Tetrahydroxy-8,3'-di(gamma,gamma-dimethylallyl)-isoflavanone

    Catalog No: CFN95084
    CAS No: 141846-47-1
    Price: $413/5mg
    Kaempferol 3-O-beta-(6''-p-coumaroyl)glucopyranosyl(1->2)-alpha-L-rhamnopyranoside

    Catalog No: CFN95089
    CAS No: 111957-48-3
    Price: $338/10mg
    Physalin O

    Catalog No: CFN95097
    CAS No: 120849-18-5
    Price: $413/5mg
    6-O-(E)-Caffeoylglucopyranose

    Catalog No: CFN95105
    CAS No: 209797-79-5
    Price: $298/5mg
    (3E,5E,11E)-tridecatriene-7,9-diyne-1,2-diacetate

    Catalog No: CFN95191
    CAS No: 94753-06-7
    Price: $318/5mg
    Batatasin V

    Catalog No: CFN95320
    CAS No: 65817-45-0
    Price: $318/5mg
    Parishin G

    Catalog No: CFN95324
    CAS No: 952283-93-1
    Price: $318/10mg
    Cannabisin M

    Catalog No: CFN95436
    CAS No: 1831134-13-4
    Price: $318/5mg
    Neoorthosiphol A

    Catalog No: CFN95447
    CAS No: 243448-72-8
    Price: $318/10mg