Hypericin CAS NO.548-04-9

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition：Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Chemical Properties of Hypericin

Cas No.	548-04-9
PubChem ID	3663	Appearance	Black-blue/black powder
Formula	C30H16O8	M.Wt	504.45
Type of Compound	Anthraquinones	Storage	Desiccate at -20°C
Synonyms	Cyclosan
Solubility	DMSO : 6.2 mg/mL (12.29 mM; Need ultrasonic and warming)
Chemical Name	9,11,13,16,18,20-hexahydroxy-5,24-dimethyloctacyclo[13.11.1.12,10.03,8.04,25.019,27.021,26.014,28]octacosa-1(26),2,4(25),5,8,10,12,14(28),15(27),16,18,20,23-tridecaene-7,22-dione
SMILES	CC1=CC(=O)C2=C(C3=C(C=C(C4=C3C5=C6C7=C(C1=C25)C(=CC(=O)C7=C(C8=C(C=C(C4=C86)O)O)O)C)O)O)O
Standard InChIKey	YDOIFHVUBCIUHF-UHFFFAOYSA-N
Standard InChI	InChI=1S/C30H16O8/c1-7-3-9(31)19-23-15(7)16-8(2)4-10(32)20-24(16)28-26-18(12(34)6-14(36)22(26)30(20)38)17-11(33)5-13(35)21(29(19)37)25(17)27(23)28/h3-6,33-38H,1-2H3
General tips	For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging	1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment.
Shipping Condition	Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Hypericin

The herb of Hypericum perforatum L.

Biological Activity of Hypericin

Description	Hypericin is a photosensitive antiviral with anticancer and antidepressant agent . It can inhibit tyrosine kinases with IC50 of 7.5 μM. It can induce both apoptosis and necrosis in a concentration and light dose-dependent fashion, and inhibit RANKL-mediated osteoclastogenesis via affecting ERK signalling in vitro and suppresses wear particle-induced osteolysis in vivo.
Targets	PKC | ERK | NF-kB | JNK | p38MAPK
In vitro	Hypericin in cancer treatment: more light on the way.[Pubmed: 11849990] Int J Biochem Cell Biol. 2002 Mar;34(3):221-41. Photodynamic therapy (PDT) has been described as a promising new modality for the treatment of cancer. PDT involves the combination of a photosensitizing agent (photosensitizer), which is preferentially taken up and retained by tumor cells, and visible light of a wavelength matching the absorption spectrum of the drug. Each of these factors is harmless by itself, but when combined they ultimately produce, in the presence of oxygen, cytotoxic products that cause irreversible cellular damage and tumor destruction. Hypericin, a powerful naturally occurring photosensitizer, is found in Hypericum perforatum plants, commonly known as St. John's wort. In recent years increased interest in Hypericin as a potential clinical anticancer agent has arisen since several studies established its powerful in vivo and in vitro antineoplastic activity upon irradiation. Investigations of the molecular mechanisms underlying Hypericin photocytotoxicity in cancer cells have revealed that this photosensitizer can induce both apoptosis and necrosis in a concentration and light dose-dependent fashion. Moreover, PDT with Hypericin results in the activation of multiple pathways that can either promote or counteract the cell death program. This review focuses on the more recent advances in the use of Hypericin as a photodynamic agent and discusses the current knowledge on the signaling pathways underlying its photocytotoxic action. The effects of hypericin on ADAMTS and p53 gene expression in MCF-7 breast cancer cells.[Pubmed: 25261644] J BUON. 2014 Jul-Sep;19(3):627-32. The purpose of this study was to determine the effects of Hypericin on MCF-7 (Michigan Cancer Foundation- 7) breast cancer cells, as it is known to exert an antitumor effect on the expression and regulation of ADAMTS1, 3, 10 and the p53 gene in breast cancer cells. METHODS AND RESULTS: MFC-7 cells were cultured and subjected separately to various doses (1, 5 and 7.5 μg /mL) Hypericin. After 24 hrs, RNA was isolated and transcribed into cDNA. Expression analysis was performed by real time (RT)-PCR and cell survival was determined by the XTT assay. While the expression of ADAMTS1 in MFC-7 cells decreased to 0.04-fold after exposure to 1 μg /mL Hypericin, the expression increased by 5.6- and 36-fold with 5 and 7.5 μg/mL, respectively. Furthermore, ADAMTS3 expression in MCF7 cells increased 3.9-fold with the use of 5 μg /mL of Hypericin. These concentrations of Hypericin did not lead to significant changes in the expression of ADAMTS10 and the p53 gene. Viability of cancer cells as evaluated by the XTT assay showed that Hypericin concentration of 7.5 μg /mL led to increased apoptosis of cancer cells. CONCLUSIONS: The increase in ADAMTS1 expression may prevent metastasis or facilitate the development of an adjuvant factor with tumor-suppressive effects. Hypericin may therefore exert its antitumor and apoptotic effects in MFC-7 cells via ADAMTS1 and ADAMTS3. Hypericin and pseudohypericin specifically inhibit protein kinase C: Possible relation to their antiretroviral activity[Pubmed: 2558652] Biochem. Biophys. Res. Commun., 1989 ,165(3):1207-12. Hypericin and pseudoHypericin which have been isolated from plants of the Hypericum family are aromatic polycyclic diones. Daniel Meruelo et. al. have reported that Hypericin and pseudoHypericin showed potent antiretroviral activity including anti-human immunodeficiency virus (1,2). However, the mechanism of these antiretroviral activities has not been clarified. METHODS AND RESULTS: In the course of screening specific inhibitors of protein kinase C we have found that both compounds specifically inhibit protein kinase C with IC50 values 1.7 micrograms/ml and 15 micrograms/ml, respectively, and show antiproliferative activity against mammalian cells. CONCLUSIONS: These data suggest that antiretroviral activity of Hypericin and pseudoHypericin could be attributable to the inhibition of some phosphorylation involved by protein kinase C during viral infection of cells.
In vivo	Solubilized hypericin and pseudohypericin from Hypericum perforatum exert antidepressant activity in the forced swimming test.[Pubmed: 9619107] Planta Med. 1998 May;64(4):291-4. METHODS AND RESULTS: It has been shown recently that the fraction IIIc of a crude extract of Hypericum perforatum, (St. John's wort) that contained both Hypericin (1) and pseudoHypericin (2), was remarkably active in the rats forced swimming test (FST) after Porsolt. However, neither of the naphthodianthrones isolated from this fraction were sufficiently effective when administered suspended in water. The solubility of 1 and 2 is remarkably increased in the presence of a fraction containing procyanidins, especially procyanidin B2, which is present also in the active Hypericum fraction IIIc. The cooperative effect of procyanidins significantly increased the in vivo effects of 1 and 2, which exhibited inverted U-shaped dose response curves, in the FST. The anti-immobility effect of solubilized 1 and 2 was antagonized by the dopamine antagonist sulpiride. CONCLUSIONS: These data indicate that naphthodianthrones are antidepressant constituents of H. perforatum and suggest that the dopaminergic system is involved in their action.

Protocol of Hypericin

Cell Research

Hypericin suppresses osteoclast formation and wear particle-induced osteolysis via modulating ERK signalling pathway.[Pubmed: 24950468] Effect of PKCα expression on Bcl-2 phosphorylation and cell death by hypericin.[Pubmed: 25300800] Apoptosis. 2014 Dec;19(12):1779-92. In order to explain the contribution of the protein kinase Cα (PKCα) in apoptosis induced by photo-activation of Hypericin (Hyp), a small interfering RNA was used for post-transcriptional silencing of pkcα gene expression. METHODS AND RESULTS: We have evaluated the influence of Hyp photo-activation on cell death in non-transfected and transfected (PKCα(-)) human glioma cells (U-87 MG). No significant differences were detected in cell survival between non-transfected and transfected PKCα(-) cells. However, the type of cell death was notably affected by silencing the pkcα gene. Photo-activation of Hyp strongly induced apoptosis in non-transfected cells, but the level of necrotic cells in transfected PKCα(-) cells increased significantly. The differences in cell death after Hyp photo-activation are demonstrated by changes in: (i) reactive oxygen species production, (ii) Bcl-2 phosphorylation on Ser70 (pBcl-2(Ser70)), (iii) cellular distributions of pBcl-2(Ser70) and (iv) cellular distribution of endogenous anti-oxidant glutathione and its co-localization with mitochondria. METHODS AND RESULTS: In summary, we suggest that post-transcriptional silencing of the pkcα gene and the related decrease of PKCα level considerably affects the anti-apoptotic function and the anti-oxidant function of Bcl-2. This implies that PKCα, as Bcl-2 kinase, indirectly protects U-87 MG cells against oxidative stress and subsequent cell death. Biochem Pharmacol. 2014 Aug 1;90(3):276-87 Osteoclast-induced bone resorption and wear-particle-induced osteolysis leads to prosthetic loosening, one of the most common causes of joint implant failure, resulting in revision surgery. Thus, inhibition of osteoclastic bone resorption, which further prevents wear particle-induced osteolysis, is a potential treatment strategy for prosthetic loosening. Here, we examined the therapeutic effect of Hypericin (HP), which was photosensitive, on osteoclastogenesis and wear particle-induced osteolysis in the absence of visible light. METHODS AND RESULTS: HP inhibited RANKL-induced osteoclast differentiation in bone marrow macrophages (BMMs) and RAW264.7 cell line without any evidence of cytotoxicity. The bone-resorbing activity of mature osteoclasts was significantly inhibited by HP. As HP has been previously reported to inhibit signalling pathway such as ERK and NF-κB in other cells, which is also important in osteoclast differentiation. We thus examined the molecular mechanism and showed that HP significantly inhibited the ERK/mitogen-activated protein kinase (MAPK) signalling pathway without affecting nuclear factor kappaB (NF-κB), c-Jun N-terminal kinase (JNK) and p38 signalling in RANKL-stimulated BMMs. Further in vivo studies revealed HP attenuated osteoclast formation and subsequently prevented wear particle-induced bone erosion. Taken together, the results suggest that HP inhibits RANKL-mediated osteoclastogenesis via affecting ERK signalling in vitro and suppresses wear particle-induced osteolysis in vivo. CONCLUSIONS: We therefore conclude that HP may be an innovative and safe alternative treatment for osteoclast-related prosthetic loosening.

Preparing Stock Solutions of Hypericin

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	1.9824 mL	9.9118 mL	19.8236 mL	39.6471 mL	49.5589 mL
5 mM	0.3965 mL	1.9824 mL	3.9647 mL	7.9294 mL	9.9118 mL
10 mM	0.1982 mL	0.9912 mL	1.9824 mL	3.9647 mL	4.9559 mL
50 mM	0.0396 mL	0.1982 mL	0.3965 mL	0.7929 mL	0.9912 mL
100 mM	0.0198 mL	0.0991 mL	0.1982 mL	0.3965 mL	0.4956 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

References on Hypericin

Hypericin suppresses osteoclast formation and wear particle-induced osteolysis via modulating ERK signalling pathway.[Pubmed:24950468]

Biochem Pharmacol. 2014 Aug 1;90(3):276-87.

Osteoclast-induced bone resorption and wear-particle-induced osteolysis leads to prosthetic loosening, one of the most common causes of joint implant failure, resulting in revision surgery. Thus, inhibition of osteoclastic bone resorption, which further prevents wear particle-induced osteolysis, is a potential treatment strategy for prosthetic loosening. Here, we examined the therapeutic effect of Hypericin (HP), which was photosensitive, on osteoclastogenesis and wear particle-induced osteolysis in the absence of visible light. HP inhibited RANKL-induced osteoclast differentiation in bone marrow macrophages (BMMs) and RAW264.7 cell line without any evidence of cytotoxicity. The bone-resorbing activity of mature osteoclasts was significantly inhibited by HP. As HP has been previously reported to inhibit signalling pathway such as ERK and NF-kappaB in other cells, which is also important in osteoclast differentiation. We thus examined the molecular mechanism and showed that HP significantly inhibited the ERK/mitogen-activated protein kinase (MAPK) signalling pathway without affecting nuclear factor kappaB (NF-kappaB), c-Jun N-terminal kinase (JNK) and p38 signalling in RANKL-stimulated BMMs. Further in vivo studies revealed HP attenuated osteoclast formation and subsequently prevented wear particle-induced bone erosion. Taken together, the results suggest that HP inhibits RANKL-mediated osteoclastogenesis via affecting ERK signalling in vitro and suppresses wear particle-induced osteolysis in vivo. We therefore conclude that HP may be an innovative and safe alternative treatment for osteoclast-related prosthetic loosening.

Effect of PKCalpha expression on Bcl-2 phosphorylation and cell death by hypericin.[Pubmed:25300800]

Apoptosis. 2014 Dec;19(12):1779-92.

In order to explain the contribution of the protein kinase Calpha (PKCalpha) in apoptosis induced by photo-activation of Hypericin (Hyp), a small interfering RNA was used for post-transcriptional silencing of pkcalpha gene expression. We have evaluated the influence of Hyp photo-activation on cell death in non-transfected and transfected (PKCalpha(-)) human glioma cells (U-87 MG). No significant differences were detected in cell survival between non-transfected and transfected PKCalpha(-) cells. However, the type of cell death was notably affected by silencing the pkcalpha gene. Photo-activation of Hyp strongly induced apoptosis in non-transfected cells, but the level of necrotic cells in transfected PKCalpha(-) cells increased significantly. The differences in cell death after Hyp photo-activation are demonstrated by changes in: (i) reactive oxygen species production, (ii) Bcl-2 phosphorylation on Ser70 (pBcl-2(Ser70)), (iii) cellular distributions of pBcl-2(Ser70) and (iv) cellular distribution of endogenous anti-oxidant glutathione and its co-localization with mitochondria. In summary, we suggest that post-transcriptional silencing of the pkcalpha gene and the related decrease of PKCalpha level considerably affects the anti-apoptotic function and the anti-oxidant function of Bcl-2. This implies that PKCalpha, as Bcl-2 kinase, indirectly protects U-87 MG cells against oxidative stress and subsequent cell death.

Hypericin in cancer treatment: more light on the way.[Pubmed:11849990]

Int J Biochem Cell Biol. 2002 Mar;34(3):221-41.

Photodynamic therapy (PDT) has been described as a promising new modality for the treatment of cancer. PDT involves the combination of a photosensitizing agent (photosensitizer), which is preferentially taken up and retained by tumor cells, and visible light of a wavelength matching the absorption spectrum of the drug. Each of these factors is harmless by itself, but when combined they ultimately produce, in the presence of oxygen, cytotoxic products that cause irreversible cellular damage and tumor destruction. Hypericin, a powerful naturally occurring photosensitizer, is found in Hypericum perforatum plants, commonly known as St. John's wort. In recent years increased interest in Hypericin as a potential clinical anticancer agent has arisen since several studies established its powerful in vivo and in vitro antineoplastic activity upon irradiation. Investigations of the molecular mechanisms underlying Hypericin photocytotoxicity in cancer cells have revealed that this photosensitizer can induce both apoptosis and necrosis in a concentration and light dose-dependent fashion. Moreover, PDT with Hypericin results in the activation of multiple pathways that can either promote or counteract the cell death program. This review focuses on the more recent advances in the use of Hypericin as a photodynamic agent and discusses the current knowledge on the signaling pathways underlying its photocytotoxic action.

Hypericin and pseudohypericin specifically inhibit protein kinase C: possible relation to their antiretroviral activity.[Pubmed:2558652]

Biochem Biophys Res Commun. 1989 Dec 29;165(3):1207-12.

Hypericin and pseudoHypericin which have been isolated from plants of the Hypericum family are aromatic polycyclic diones. Daniel Meruelo et. al. have reported that Hypericin and pseudoHypericin showed potent antiretroviral activity including anti-human immunodeficiency virus (1,2). However, the mechanism of these antiretroviral activities has not been clarified. In the course of screening specific inhibitors of protein kinase C we have found that both compounds specifically inhibit protein kinase C with IC50 values 1.7 micrograms/ml and 15 micrograms/ml, respectively, and show antiproliferative activity against mammalian cells. These data suggest that antiretroviral activity of Hypericin and pseudoHypericin could be attributable to the inhibition of some phosphorylation involved by protein kinase C during viral infection of cells.

The effects of hypericin on ADAMTS and p53 gene expression in MCF-7 breast cancer cells.[Pubmed:25261644]

J BUON. 2014 Jul-Sep;19(3):627-32.

PURPOSE: The purpose of this study was to determine the effects of Hypericin on MCF-7 (Michigan Cancer Foundation- 7) breast cancer cells, as it is known to exert an antitumor effect on the expression and regulation of ADAMTS1, 3, 10 and the p53 gene in breast cancer cells. METHODS: MFC-7 cells were cultured and subjected separately to various doses (1, 5 and 7.5 mug /mL) Hypericin. After 24 hrs, RNA was isolated and transcribed into cDNA. Expression analysis was performed by real time (RT)-PCR and cell survival was determined by the XTT assay. RESULTS: While the expression of ADAMTS1 in MFC-7 cells decreased to 0.04-fold after exposure to 1 mug /mL Hypericin, the expression increased by 5.6- and 36-fold with 5 and 7.5 mug/mL, respectively. Furthermore, ADAMTS3 expression in MCF7 cells increased 3.9-fold with the use of 5 mug /mL of Hypericin. These concentrations of Hypericin did not lead to significant changes in the expression of ADAMTS10 and the p53 gene. Viability of cancer cells as evaluated by the XTT assay showed that Hypericin concentration of 7.5 mug /mL led to increased apoptosis of cancer cells. CONCLUSION: The increase in ADAMTS1 expression may prevent metastasis or facilitate the development of an adjuvant factor with tumor-suppressive effects. Hypericin may therefore exert its antitumor and apoptotic effects in MFC-7 cells via ADAMTS1 and ADAMTS3.

Solubilized hypericin and pseudohypericin from Hypericum perforatum exert antidepressant activity in the forced swimming test.[Pubmed:9619107]

Planta Med. 1998 May;64(4):291-4.

It has been shown recently that the fraction IIIc of a crude extract of Hypericum perforatum, (St. John's wort) that contained both Hypericin (1) and pseudoHypericin (2), was remarkably active in the rats forced swimming test (FST) after Porsolt. However, neither of the naphthodianthrones isolated from this fraction were sufficiently effective when administered suspended in water. The solubility of 1 and 2 is remarkably increased in the presence of a fraction containing procyanidins, especially procyanidin B2, which is present also in the active Hypericum fraction IIIc. The cooperative effect of procyanidins significantly increased the in vivo effects of 1 and 2, which exhibited inverted U-shaped dose response curves, in the FST. The anti-immobility effect of solubilized 1 and 2 was antagonized by the dopamine antagonist sulpiride. These data indicate that naphthodianthrones are antidepressant constituents of H. perforatum and suggest that the dopaminergic system is involved in their action.

Inhibition of c-erbB-2 expression an activity in human ovarian carcinoma cells by hypericin.[Pubmed:11724334]

Anticancer Res. 2001 Jul-Aug;21(4A):2649-55.

The c-erbB-2 oncogene encodes a tyrosine kinase that constitutes the internal and transmembrane part of the epidermal growth factor receptor (EGFR). ErbB-2 overexpression has been reported in 20% to 30% of human adenocarcinomas of the breast and ovary, and has been linked to an unfavorable prognosis in patients. Hypericin is a protein tyrosine kinase inhibitor that has been exploited in models for anti-tumor and anti-viral activity. In this study, we investigated the effects of Hypericin on the activity of the c-erbB-2 oncoprotein and its downstream kinases. We also investigated the effect of Hypericin on metastasis. We used ovarian SK-OV-3 cells as a model to determine whether Hypericin-induced cell death was associated with inhibition of c-erbB-2 expression and activation. The IC50 of Hypericin after 72 hrs exposure was 7.5 microM as determined by the MTT assay. Apoptosis, which was assessed by morphological changes and a flow cytometric assay, was observed at 24 h after continuous exposure to 5 microM Hypericin. Inhibition of expression of the c-erbB-2 protein was detected, using a monoclonal anti-erbB-2 antibody after 12-48 hrs of exposure to Hypericin. Hypericin was found to inhibit autophosphorylation of the erbB-2 protein and downstream kinases such as MEK and ERK1/2. We also found up-regulation of p21WAF1 expression and down-regulation of Bcl-2 in Hypericin treated cells. An invasion assay showed that Hypericin inhibited the movement of SK-OV-3 cells into the Matrigel. However, gelatin zymography showed that Hypericin had no effect on the secretion of matrix metalloproteinases (MMPs) in SK-OV-3 cells. From these results, we conclude that Hypericin inhibits the growth of SK-OV-3 ovarian cancer cells, inhibits the autophosphorylation of c-erbB-2, induces apoptosis, and may inhibit invasion.

Photodynamic inactivation of infectivity of human immunodeficiency virus and other enveloped viruses using hypericin and rose bengal: inhibition of fusion and syncytia formation.[Pubmed:7678335]

Proc Natl Acad Sci U S A. 1993 Jan 1;90(1):158-62.

The mechanism of the antiviral activity of Hypericin was characterized and compared with that of rose bengal. Both compounds inactivate enveloped (but not unenveloped) viruses upon illumination by visible light. Human immunodeficiency and vesicular stomatitis viruses were photodynamically inactivated by both dyes at nanomolar concentrations. Photodynamic inactivation of fusion (hemolysis) by vesicular stomatitis, influenza, and Sendai viruses was induced by both dyes under similar conditions (e.g., I50 = 20-50 nM for vesicular stomatitis virus), suggesting that loss of infectivity resulted from inactivation of fusion. Syncytium formation, between cells activated to express human immunodeficiency virus gp120 on their surfaces and CD4+ cells, was inhibited by illumination in the presence of 1 microM Hypericin. Hypericin and rose bengal thus exert similar virucidal effects. Both presumably act by the same mechanism--namely, the inactivation of the viral fusion function by singlet oxygen produced upon illumination. The implications of this photodynamic antiviral action for the potential therapeutic usefulness of both Hypericin and rose bengal are discussed.

Description

Hypericin is a photosensitive antiviral with anticancer and antidepressant agent derived from Hypericum perforatum.

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