yingweiwo

Pseudohypericin

Cat No.:V34238 Purity: ≥98%
Pseudohypericin and its homolog Hypericin are the major hydroxyphenanthrolinones in Hypericum.
Pseudohypericin
Pseudohypericin Chemical Structure CAS No.: 55954-61-5
Product category: Natural Products
This product is for research use only, not for human use. We do not sell to patients.
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Product Description
Pseudohypericin and its homolog Hypericin are the major hydroxyphenanthrolinones in Hypericum. Pseudohypericin has anti-HIV (Human Immunodeficiency Virus) activity.
Biological Activity I Assay Protocols (From Reference)
ln Vitro
Antiretroviral activity is present in pseudohyperin [1].
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Hypericins, hyperforin and flavonoids are discussed as the main components contributing to the antidepressant action of St. John's wort (Hypericum perforatum). Therefore, the objective of the two open phase I clinical trials was to obtain pharmacokinetic data of these constituents from a hypericum extract containing tablet: hypericin, pseudohypericin, hyperforin, the flavonoid aglycone quercetin, and its methylated form isorhamnetin. Each trial included 18 healthy male volunteers who received the test preparation, containing 900 mg dry extract of St John's wort (STW 3-VI, Laif 900), either as a single oral dose or as a multiple once daily dose over a period of 14 days. Concentration/time curves were determined for the five constituents, for 48 hr after single dosing and for 24 hr on day 14 at the end of 2 weeks of continuous daily dosing. After single dose intake, the key pharmacokinetic parameters were determined as follows: ...pseudohypericin: AUC(0-infinity) = 97.28 hr x ng/mL, Cmax = 10.2 ng/mL, tmax = 2.7 hr, elimination half-life 17.19 hr... Under steady state conditions reached during multiple dose administration similar results were obtained. Further pharmacokinetic characteristics calculated from the obtained data were the mean residence time (MRT), the lag-time, the peak-trough fluctuation (PTF), the lowest observed plasma concentration (Cmin), and the average plasma concentration (Cav). The data obtained for the five consitituents generally corresponded well with values previously published. The trial preparation was well tolerated.
The objective of these two open phase I clinical trials was the investigation of the bioavailability of five constituents from a hypericum extract containing tablet, which are discussed as the components contributing to the antidepressant action. Each trial included 18 healthy male volunteers who received the test preparation, containing 612 mg dry extract of St John's wort (STW-3, Laif 600), either as a single oral dose or as a multiple once daily dose over a period of 14 days. Concentration/time curves were determined for hypericin, pseudohypericin, hyperforin, the flavonoid aglycone quercetin, and its methylated form isorhamnetin for 48 hr after single dosing and for 24 hr on day 14 at the end of 2 weeks of continuous daily dosing. After single dose intake, the key pharmacokinetic parameters were determined as follows: ...pseudohypericin: AUC(0-infinity) = 93.03 hr x ng/mL, Cmax = 8.50 ng/mL, t(max) = 3.0 hr, elimination half-life 25.39 hr... Under steady state conditions reached during multiple dose administration similar results were obtained. Further pharmacokinetic characteristics calculated from the obtained data were the mean residence time (MRT), the lag-time, the peak-trough fluctuation (PTF), the lowest observed plasma concentration (Cmin), and the average plasma concentration (Cav). The data obtained for hypericin, pseudohypericin and hyperforin generally corresponded well with values previously published, with some deviations observed for the extent of absorption of hypericin and the time course of absorption and elimination of hyperforin. ...The trial preparation was well tolerated.
Extracts of St. John's wort (Hypericum perforatum) are used in treatment of depression. They contain various substances with the naphthodianthrones hypericin and pseudohypericin as characteristic ingredients. These compounds were shown to cause phototoxicity in cell culture and in animals. A placebo-controlled randomized clinical trial with monitoring of hypericin and pseudohypericin plasma concentration was performed to evaluate the increase in dermal photosensitivity in humans after application of high dose hypericum extracts. The study was divided into a single dose and a multiple dose part. In the single dose period, each of 13 volunteers received in a double blind fourfold complete crossover design, either placebo, or 900, 1800 or 3600 mg of a standardized hypericum extract (LI 160) containing zero, 2.81, 5.62 and 11.25 mg of total hypericin (total hypericin is the sum of hypericin and pseudohypericin). Maximum total hypericin plasma concentrations were observed about 4 hr after dosage and were 0, 0.028, 0.061 and 0.159 mg/L, respectively...
This study evaluated the influence of cimetidine and carbamazepine on the pharmacokinetics of the St. John's Wort (SJW) ingredients hypericin and pseudohypericin. In a placebo-controlled, double blind study, 33 healthy volunteers were randomized into three treatment groups that received SJW extract (LI160) with different comedications (placebo, cimetidine, and carbamazepine) for 7 days after a run-in period of 11 days with SJW alone. Hypericin and pseudohypericin pharmacokinetics were measured on days 10 and 17. Between-group comparisons showed no statistically significant differences in AUC(0-24), C(max), and t(max) values for hypericin and pseudohypericin. Within-group comparisons, however, revealed a statistically significant increase in hypericin AUC(0-24) from a median of 119 (range 82-163 ug hr/L) to 149 ug hr/L (61-202 ug hr/L) with cimetidine comedication and a decrease in pseudohypericin AUC(0-24) from a median of 51.0 (16.4-102.9 ug hr/L) to 36.4 ug hr/L (14.0-102.0 ug hr/L) with carbamazepine comedication compared to the baseline pharmacokinetics in each group. Hypericin and pseudohypericin pharmacokinetics were only marginally influenced by comedication with the enzyme inhibitors and inducers cimetidine and carbamazepine.
To study the single dose and steady state pharmacokinetics of hypericin and pseudohypericin, a study was conducted in 13 healthy male volunteers, ages 25-30 yr, who received an oral extract of St. John's Worts LI 160. Oral administration of 250, 750, and 1500 ug of hypericin and 526, 1578, and 3156 ug of pseudohypericin resulted in median peak plasma levels (Cmax) of 1.3, 7.2, and 16.6 ug/L for hypericin and 3.4, 12.1, and 29.7 ug/L for pseudohypericin, respectively. Cmax and AUC values for the lowest dose were disproportionally lower than those for the higher doses. A lag time of 1.9 hr for hypericin was remarkably longer than the 0.4 hr lag time for pseudohypericin. Median half-lives for absorption, distribution, and elimination were 0.6, 6, and 43.1 hr after 750 ug of hypericin and 1.3, 1.4, and 24.8 hr after 1578 ug of pseudohypericin, respectively; the corresponding Cmax levels were 8.8 and 8.5 ug/L. Both hypericin and pseudohypericin were initially distributed into a central volume of 4.2 and 5 L, respectively. The systemic availability of hypericin and pseudohypericinfrom the extract was 14 and 21%, respectively.
Biological Half-Life
Median half-lives for absorption, distribution, and elimination were 0.6, 6, and 43.1 hr after 750 ug of hypericin and 1.3, 1.4, and 24.8 hr after 1578 ug of pseudohypericin, respectively...
Each trial included 18 healthy male volunteers who received the test preparation, containing 900 mg dry extract of St John's wort (STW 3-VI, Laif 900), either as a single oral dose or as a multiple once daily dose over a period of 14 days. Concentration/time curves were determined for the five constituents, for 48 hr after single dosing and for 24 hr on day 14 at the end of 2 weeks of continuous daily dosing. After single dose intake, the key pharmacokinetic parameters were determined as follows: ...pseudohypericin: ...elimination half-life 17.19 hr... Under steady state conditions reached during multiple dose administration similar results were obtained.
Each trial included 18 healthy male volunteers who received the test preparation, containing 612 mg dry extract of St John's wort (STW-3, Laif 600), either as a single oral dose or as a multiple once daily dose over a period of 14 days. After single dose intake, the key pharmacokinetic parameters were determined as follows: ...pseudohypericin: elimination half-life 25.39 hr... Under steady state conditions reached during multiple dose administration similar results were obtained...
Toxicity/Toxicokinetics
Interactions
St John's wort reduced the area under the curve of the HIV-1 protease inhibitor indinavir by a mean of 57% (SD 19) and decreased the extrapolated 8-hr indinavir trough by 81% (16) in healthy volunteers. A reduction in indinavir exposure of this magnitude could lead to the development of drug resistance and treatment failure /St John's wort/.
Hypericum perforatum (Hp) has been used medicinally to treat a variety of conditions including mild-to-moderate depression. Recently, several anti-inflammatory activities of Hp have been reported. An ethanol extract of Hp was fractionated with the guidance of an anti-inflammatory bioassay (lipopolysaccharide (LPS)-induced prostaglandin E2 production (PGE2)), and four constituents were identified. When combined together at concentrations detected in the Hp fraction to make a 4 component system, these constituents (0.1 uM chlorogenic acid (compound 1), 0.08 uM amentoflavone (compound 2), 0.07 uM quercetin (compound 3), and 0.03 uM pseudohypericin (compound 4)) explained the majority of the activity of the fraction when activated by light, but only partially explained the activity of this Hp fraction in dark conditions. One of the constituents, light-activated pseudohypericin, was necessary, but not sufficient to explain the reduction in LPS-induced PGE2 of the 4 component system. The Hp fraction and the 4 component system inhibited lipoxygenase and cytosolic phospholipase A2, two enzymes in the PGE2-mediated inflammatory response. The 4 component system inhibited the production of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and the Hp fraction inhibited the anti-inflammatory cytokine interleukin-10 (IL-10). Thus, the Hp fraction and selected constituents from this fraction showed evidence of blocking pro-inflammatory mediators but not enhancing inflammation-suppressing mediators.
/The authors/ evaluated the pharmacokinetic interaction between a low-hyperforin St John's wort (SJW) extract and alprazolam, caffeine, tolbutamide, and digoxin. Previous reports on other SJW products had shown remarkably decreased plasma concentrations of certain co-medicated drugs, which was attributed to an inducing effect of SJW on cytochrome P-450 (CYP) and p-glycoprotein (p-gp) activity. Two randomised, placebo-controlled studies were performed with 28 healthy volunteers (age 18 - 55 years) in each study. In study A, single doses of alprazolam (1 mg; substrate of CYP3A4) and caffeine (100 mg; CYP1A2) were given on days 1 and 11. In study B, single doses of tolbutamide (500 mg, days 1 and 11; CYP2C9) and multiple doses of digoxin (0.75 mg on days -2 and -1, 0.25 mg /per day/ on days 1 to 11; p-gp) were given. The participants received SJW (Esbericum capsules; 240 mg /per day/ of extract, 3.5 mg hyperforin) or placebo on days 2 to 11. Blood for pharmacokinetic analysis was drawn on days 1 and 11. No statistically significant differences were found in the primary kinetic parameter, AUC0 - 24, of alprazolam, caffeine (AUC0 - 12), paraxanthine, tolbutamide, 4-hydroxytolbutamide, and digoxin between the placebo group and the SJW group at the end of the study. The SJW-induced change in AUCs was less than 12 % of the initial median AUC of the participants in studies A and B, thus clinically irrelevant. On day 11, trough concentrations were 2.0 (range 0.6 - 4.1) ug/L and 1.0 (0.2 - 3.9) ug/L for hypericin and pseudohypericin, respectively, whereas hyperforin concentrations were below the quantification limit (< 1 ug/L). Kinetics of investigated probe drugs were only marginally influenced by concomitant treatment with Esbericum capsules. This may be due in particular to the low hyperforin plasma concentration as this SJW component has been shown to activate the PXR receptor which regulates expression of CYP3A4 and p-gp...
The present interest and widespread use of herbal remedies has created the possibility of interaction between them and pharmaceutical drugs if they are used simultaneously. Before the recent reports of apparent hepatotoxicity associated with its use, kava (Piper methysticum Forst. F.), was one of the top 10 selling herbal remedies in Europe and North America. This adverse effect was not previously encountered with the traditional beverage which was prepared as a water infusion in contrast to the commercial products which are extracted with organic solvents. Kavalactones, the active principles in kava, are potent inhibitors of several of the CYP 450 enzymes, suggesting a high potential for causing pharmacokinetic interactions with drugs and other herbs which are metabolized by the same CYP 450 enzymes. Furthermore, some kavalactones have been shown to possess pharmacological effects, such as blockade of GABA receptors and sodium and calcium ion channels, which may lead to pharmacodynamic interactions with other substances which possess similar pharmacological proprieties. St. John's wort (Hypericum perforatum L.), used extensively for the treatment of mild to moderate clinical depression, has long been considered safer than the conventional pharmaceutical agents. However, its ability, through its active constituents hypericin, pseudohypericin and hyperforin, to induce intestinal P-glycoprotein/MRD1 and both intestinal and hepatic CYP3A4 enzyme, could markedly reduce the distribution and disposition of their co-substrates. In addition, St. John's wort is a potent uptake inhibitor of the neurotransmitters serotonin, norepinephrine and dopamine all of which have a role in mood control. Consequently, the very real potential for a pharmacodynamic interaction between the herb and pharmaceutical drugs which share this mechanism of action and, like St. John's wort, are used for mood elevation. However, presently there is very little evidence to substantiate actual pharmacokinetic and/or pharmacodynamic interaction between drugs and kava or St. John's wort. This review provides a brief overview of the existing data on interactions of kava and St. John's wort with pharmaceutical agents and as a result reveals the urgent need for detailed investigations to identify clinically significant interactions for these herbal remedies that have the potential to cause adverse effects.
For more Interactions (Complete) data for Pseudohypericin (8 total), please visit the HSDB record page.
References

[1]. Studies of the mechanisms of action of the antiretroviral agents hypericin and pseudohypericin. Proc Natl Acad Sci U S A. 1989 Aug;86(15):5963-7.

[2]. Apoptosis of THP-1 Macrophages Induced by Pseudohypericin-Mediated Sonodynamic Therapy Through the Mitochondria-Caspase Pathway. Cell Physiol Biochem. 2016;38(2):545-57.

Additional Infomation
Pseudohypericin is an ortho- and peri-fused polycyclic arene.
Pseudohypericin has been reported in Hypericum tomentosum, Hypericum montanum, and other organisms with data available.
Mechanism of Action
Cytosolic (TrxR1) and mitochondrial (TrxR2) thioredoxin reductases experience pronounced concentration- and time-dependent inhibition when incubated with the two naphthodianthrones hypericin and pseudohypericin. Pseudohypericin turned out to be a quite strong inhibitor of TrxR1 (IC(50)=4.40uM) being far more effective than hypericin (IC(50)=157.08uM). In turn, the IC(50) values measured toward TrxR2 were 7.45uM for pseudohypericin and 43.12uM for hypericin. When compared to pseudohypericin, the inhibition caused by hypericin usually required significantly longer times, in particular on TrxR1. These important differences in the inhibitory potencies and profiles were analysed through a molecular modeling approach. Notably, both compounds were found to accommodate in the NADPH-binding pocket of the enzyme. The binding of the two naphthodianthrones to thioredoxin reductase seems to be particularly strong as the inhibitory effects were fully retained after gel filtration. Also, we found that TrxR inhibition by hypericin and pseudohypericin does not involve the active site selenol/thiol motif as confirmed by biochemical and modeling studies. The resulting inhibition pattern is very similar to that produced by the two naphthodianthrones on glutathione reductase. As the thioredoxin system is highly overexpressed in cancer cells, its inhibition by hypericin and pseudohypericin, natural compounds showing appreciable anticancer properties, might offer new clues on their mechanism of action and open interesting perspectives for future tumor therapies.
Therapeutic Uses
Antiviral Agents; Enzyme Inhibitors
/EXPERIMENTAL THER/ Two aromatic polycyclic diones hypericin and pseudohypericin have potent antiretroviral activity; these substances occur in plants of the Hypericum family. Both compounds are highly effective in preventing viral-induced manifestations that follow infections with a variety of retroviruses in vivo and in vitro. Pseudohypericin and hypericin probably interfere with viral infection and/or spread by direct inactivation of the virus or by preventing virus shedding, budding, or assembly at the cell membrane. These compounds have no apparent activity against the transcription, translation, or transport of viral proteins to the cell membrane and also no direct effect on the polymerase. This property distinguishes their mode of action from that of the major antiretro-virus group of nucleoside analogues. Hypericin and pseudohypericin have low in vitro cytotoxic activity at concentrations sufficient to produce dramatic antiviral effects in murine tissue culture model systems that use radiation leukemia and Friend viruses. Administration of these compounds to mice at the low doses sufficient to prevent retroviral-induced disease appears devoid of undesirable side effects. This lack of toxicity at therapeutic doses extends to humans, as these compounds have been tested in patients as antidepressants with apparent salutary effects. /These/ observations to date suggest that pseudohypericin and hypericin could become therapeutic tools against retroviral-induced diseases such as acquired immunodeficiency syndrome (AIDS).
St. John's wort (Hypericum perforatum L.), used extensively for the treatment of mild to moderate clinical depression, has long been considered safer than the conventional pharmaceutical agents.
Drug Warnings
In the United States, /St. John's wort (SJW), known botanically as Hypericum perforatum/, like all herbal remedies, is listed as a dietary supplement by the Food and Drug Administration (FDA). Therefore, it is not subject to the strict scrutiny for safety and efficacy that standard pharmaceutical drugs are required to pass...
...concomitant administration of St. John's wort and indinavir substantially decreased indinavir plasma concentrations, potentially due to induction of the cytochrome P450 metabolic pathway. ...pharmacokinetic data are available only for concomitant administration of indinavir with St. John's wort. However, based on these results, it is expected that St John's wort may significantly decrease blood concentrations of all of the currently marketed HIV protease inhibitors (PIs) and possibly other drugs (to varying degrees) that are similarly metabolized, including the nonnucleoside reverse transcriptase inhibitors (NNRTIs). Consequently, concomitant use of St John's wort with PIs or NNRTIs is not recommended because this may result in suboptimal antiretroviral drug concentrations, leading to loss of virologic response and development of resistance or class cross-resistance /St. John's wort/.
St. John's wort (Hypericum perforatum L.), used extensively for the treatment of mild to moderate clinical depression, has long been considered safer than the conventional pharmaceutical agents. However, its ability, through its active constituents hypericin, pseudohypericin and hyperforin, to induce intestinal P-glycoprotein/MRD1 and both intestinal and hepatic CYP3A4 enzyme, could markedly reduce the distribution and disposition of their co-substrates. In addition, St. John's wort is a potent uptake inhibitor of the neurotransmitters serotonin, norepinephrine and dopamine all of which have a role in mood control. Consequently, the very real potential for a pharmacodynamic interaction between the herb and pharmaceutical drugs which share this mechanism of action and, like St. John's wort, are used for mood elevation.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C30H16O9
Molecular Weight
520.4426
Exact Mass
520.079
CAS #
55954-61-5
PubChem CID
4978
Appearance
Brown to black Solid
Density
2.0±0.1 g/cm3
Boiling Point
994.7±65.0 °C at 760 mmHg
Flash Point
569.2±30.8 °C
Vapour Pressure
0.0±0.3 mmHg at 25°C
Index of Refraction
2.169
LogP
6.75
Hydrogen Bond Donor Count
7
Hydrogen Bond Acceptor Count
9
Rotatable Bond Count
1
Heavy Atom Count
39
Complexity
1190
Defined Atom Stereocenter Count
0
SMILES
O([H])C1C2=C(C([H])=C(C3C4C(=C([H])C(=C5C(=C6C(C([H])=C(C([H])([H])[H])C7=C8C(C([H])([H])O[H])=C([H])C(C=1C8=C(C=32)C(C=45)=C76)=O)=O)O[H])O[H])O[H])O[H])O[H]
InChi Key
NODGUBIGZKATOM-UHFFFAOYSA-N
InChi Code
InChI=1S/C30H16O9/c1-7-2-9(32)19-23-15(7)16-8(6-31)3-10(33)20-24(16)28-26-18(12(35)5-14(37)22(26)30(20)39)17-11(34)4-13(36)21(29(19)38)25(17)27(23)28/h2-5,31,34-39H,6H2,1H3
Chemical Name
9,11,13,16,18,20-hexahydroxy-5-(hydroxymethyl)-24-methyloctacyclo[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
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
Solubility (In Vivo)
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

Injection Formulations
(e.g. IP/IV/IM/SC)
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution 50 μL Tween 80 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO 400 μLPEG300 50 μL Tween 80 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).
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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO 100 μLPEG300 200 μL castor oil 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (i.e. 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH 400 μLPEG300 50 μL Tween 80 450 μL Saline)


Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).
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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders


Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 1.9215 mL 9.6073 mL 19.2145 mL
5 mM 0.3843 mL 1.9215 mL 3.8429 mL
10 mM 0.1921 mL 0.9607 mL 1.9215 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

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