| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| 5mg |
|
||
| 100mg | |||
| Other Sizes |
| Targets |
Sterigmatocystin is a mycotoxin that inhibits DNA, RNA, and protein synthesis by intercalating into DNA. It is an inhibitor of G1 phase and DNA synthesis and is used to inhibit p21 activity. The compound activates ATM, p53, and Chk2 and damages DNA, inducing G2 phase cell cycle arrest. Sterigmatocystin is also an acyl-CoA:cholesterol acyltransferase 2 (ACAT2) inhibitor. Its mechanism of action involves DNA damage and cell cycle arrest. The compound is structurally related to the aflatoxins and is considered mutagenic, teratogenic, and carcinogenic.
|
|---|---|
| ln Vitro |
Variegated cystine-induced DNA damage triggers the ATM/53-dependent signaling pathway, which in turn helps GES-1 cells enter G2 arrest [4].
In vitro, Sterigmatocystin intercalates into DNA, leading to cellular damage and oxidative stress. It inhibits DNA, RNA, and protein synthesis. The compound activates ATM, p53, and Chk2 and damages DNA, inducing G2 phase cell cycle arrest. Sterigmatocystin is a DNA synthesis inhibitor and exhibits cytotoxic, carcinogenic, and mutagenic activities. Its in vitro activity is characterized by potent DNA damaging and cell cycle arresting effects. It is used as a research tool to study DNA damage response and carcinogenesis. |
| ln Vivo |
p21WAF1/CIP1 is inhibited by meterocystine (ip; 3 mg/kg once daily for 14 days) [3].
In vivo, Sterigmatocystin has teratogenic and carcinogenic effects in animals. It is a mycotoxin produced by Aspergillus species and is a food contaminant of concern. The compound uncouples oxidative phosphorylation but, unlike the aflatoxins, does not induce mitochondrial swelling or hinder Ca2+-induced swelling of mitochondria. Its in vivo toxicity is well-documented, and it is used in toxicological research to study the effects of mycotoxins. Sterigmatocystin is not used therapeutically. |
| Enzyme Assay |
In vitro enzyme/receptor binding assays for Sterigmatocystin typically involve studying its interaction with DNA. The compound intercalates into DNA, and its binding can be assessed using spectroscopic techniques such as UV-Vis or fluorescence spectroscopy. These assays confirm the compound's mechanism of action as a DNA intercalator. Sterigmatocystin's effects on DNA synthesis can be assessed using cell-free DNA polymerase assays. Its ability to activate ATM, p53, and Chk2 can be studied using kinase assays.
|
| Cell Assay |
In vitro cellular assays for Sterigmatocystin typically involve treating cells with the compound and measuring DNA damage, cell cycle arrest, and apoptosis. The compound activates ATM, p53, and Chk2 and induces G2 phase cell cycle arrest. It inhibits DNA, RNA, and protein synthesis. These cell-based studies demonstrate the compound's genotoxic and cytotoxic effects. Sterigmatocystin is used as a research tool to study DNA damage response and carcinogenesis.
|
| Animal Protocol |
In vivo animal models for Sterigmatocystin typically involve administering the compound to rodents to study its carcinogenic and teratogenic effects. The compound is administered by appropriate routes, and tumor formation or developmental abnormalities are assessed. Sterigmatocystin's in vivo toxicity is well-documented, and it is used in toxicological research to study the effects of mycotoxins. Doses and administration routes are optimized based on the specific model and experimental endpoints.
|
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Following a single intraperitoneal injection of 6.4 mg/rat (14)C-ochratoxin DMSO solution, 5.6% activity was detected in urine 12 hours later, 67% in feces and the gastrointestinal tract, and 11% in the liver. These levels decreased slightly after 24 hours. In fasted or non-fasted rats, the highest activity was observed in feces and the gastrointestinal tract 16 hours after oral administration of 1.4 mg/rat (3)H-ochratoxin; lower levels were detected in urine, blood, exhaled breath, liver, and kidneys. Metabolism/Metabolites In green monkeys, the major urinary metabolite was identified as ochratoxin-β-D-glucuronide, accounting for 75% of the oral dose. Ochratoxin covalently bound to calf thymus DNA upon incubation with phenobarbital-induced rat liver microsomes. The adduct was identified as 1,2-dihydro-2-(N7-guanosyl)-1-hydroxyochratoxin. The structure and stereochemistry of the adduct indicate that exo-ochratoxin-1,2-oxide is a metabolite reacting with DNA, and the quantitative yield of the adduct suggests that this metabolite is the major product of ochratoxin metabolism in vitro. The order of ochratoxin toxicity sensitivity among different species is: monkey > rat > mouse. It is speculated that these differences are due to variations in the distribution of ochratoxin in the liver of different species, differences in the formation of ochratoxin 2,3-epoxide from ochratoxin, and differences in drug-metabolizing enzymes in liver microsomes. Ochratoxin is activated by the human P450 enzyme CYP3A4. (From table) Sterigmatocystin has a molecular formula of C18H12O6 and a molecular weight of 324.29 g/mol. It is a mycotoxin produced by several species of Aspergillus. The compound is typically stored under appropriate conditions to maintain stability. Its physicochemical properties support its use in toxicological research. Sterigmatocystin is a known carcinogen and should be handled with extreme caution in laboratory settings. |
| Toxicity/Toxicokinetics |
Non-Human Toxicity Values
LD50 Monkey (African green monkey) Intraperitoneal injection: 32 mg/kg body weight, soluble in dimethyl sulfoxide. LD50 Rat (male) Oral administration (10 days): 166 mg/kg body weight, soluble in dimethylformamide. LD50 Rat (female) Oral administration (10 days): 120 mg/kg body weight, soluble in wheat germ oil. LD50 Rat (male) Intraperitoneal injection: 60-65 mg/kg body weight, depending on the solvent used. LD50 Mouse Oral administration: 800 mg/kg Sterigmatocystin is a highly toxic compound with mutagenic, teratogenic, and carcinogenic properties. It is a mycotoxin that poses a significant health risk through food contamination. The compound should be handled with extreme caution in laboratory settings, and appropriate safety measures, including the use of personal protective equipment, should be employed. Its toxicity is well-documented, and it is classified as a potential human carcinogen. |
| References |
[1]. Kusunoki M, et al. Long-term administration of the fungus toxin, sterigmatocystin, induces intestinal metaplasia and increases the proliferative activity of PCNA, p53, and MDM2 in the gastric mucosa of aged Mongolian gerbils. Environ Health Prev Med. 2011 Jul;16(4):224-31.
[2]. Schroeder HW, et al. Production of sterigmatocystin by some species of the genus Aspergillus and its toxicity to chicken embryos. Appl Microbiol. 1975 Oct;30(4):589-91. [3]. Tong YF, et al. Cyclin-Dependent Kinase Inhibitor p21WAF1/CIP1 Facilitates the Development of CardiacHypertroph. Cell Physiol Biochem. 2017;42(4):1645-1656. [4]. Zhang D, et al. Sterigmatocystin-induced DNA damage triggers G2 arrest via an ATM/p53-related pathway in human gastric epithelium GES-1 cells in vitro. PLoS One. 2013 May 21;8(5):e65044. |
| Additional Infomation |
According to an independent committee of scientific and health experts, ochratoxin may be carcinogenic. Ochratoxin is an organic heteropentacyclic compound with a skeleton formed by the ortho-fusion of a xanthine ring system and a dihydrofuran moiety. It is the parent compound of ochratoxins. It is a metabolite. Its function is related to dihydrodemethylochratoxin. Ochratoxin has been reported in Aspergillus amstrodamycin, Aspergillus polychromaticus, and several other organisms with relevant data. Ochratoxin is a carcinogenic fungal toxin produced in large quantities by common mold strains, Aspergillus polychromaticus, Aspergillus nidus, and an unidentified Dipolaris fungus. It can cause liver and kidney necrosis and inhibit orotic acid incorporation into nuclear RNA.
Sterigmatocystin (CAS# 10048-13-2) is a mycotoxin produced by several species of Aspergillus and is structurally related to the aflatoxins. It is a precursor of aflatoxin B1 and is an inhibitor of G1 phase and DNA synthesis. Sterigmatocystin inhibits DNA, RNA, and protein synthesis by intercalating into DNA. It is mutagenic, teratogenic, and carcinogenic. The compound is for research use only and is not approved for human therapeutic use. It should be handled with extreme caution due to its high toxicity. |
| Molecular Formula |
C18H12O6
|
|---|---|
| Molecular Weight |
324.28
|
| Exact Mass |
324.063
|
| CAS # |
10048-13-2
|
| PubChem CID |
5280389
|
| Appearance |
Pale-yellow crystals
|
| Density |
1.5±0.1 g/cm3
|
| Boiling Point |
569.7±50.0 °C at 760 mmHg
|
| Melting Point |
246ºC with decomp
|
| Flash Point |
215.9±23.6 °C
|
| Vapour Pressure |
0.0±1.6 mmHg at 25°C
|
| Index of Refraction |
1.686
|
| LogP |
1.62
|
| Hydrogen Bond Donor Count |
1
|
| Hydrogen Bond Acceptor Count |
6
|
| Rotatable Bond Count |
1
|
| Heavy Atom Count |
24
|
| Complexity |
562
|
| Defined Atom Stereocenter Count |
2
|
| SMILES |
O=C1C2=C(OC3=C1C(O)=CC=C3)C4=C(O[C@]5([H])[C@@]4([H])C=CO5)C=C2OC
|
| InChi Key |
UTSVPXMQSFGQTM-DCXZOGHSSA-N
|
| InChi Code |
InChI=1S/C18H12O6/c1-21-11-7-12-13(8-5-6-22-18(8)24-12)17-15(11)16(20)14-9(19)3-2-4-10(14)23-17/h2-8,18-19H,1H3/t8-,18+/m0/s1
|
| Chemical Name |
(3S,7R)-15-hydroxy-11-methoxy-6,8,20-trioxapentacyclo[10.8.0.02,9.03,7.014,19]icosa-1,4,9,11,14,16,18-heptaen-13-one
|
| Synonyms |
NSC-201423; Sterigmatocystine; Sterigmatocystin
|
| 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: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ~25 mg/mL (~77.09 mM)
|
|---|---|
| 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
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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 : PEG300 ：Tween 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). View More
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)] 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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.0838 mL | 15.4188 mL | 30.8375 mL | |
| 5 mM | 0.6168 mL | 3.0838 mL | 6.1675 mL | |
| 10 mM | 0.3084 mL | 1.5419 mL | 3.0838 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.
Calculation results
Working concentration： mg/mL；
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.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
