Cytochrome P450 3A4/5 ELISA Kit

Name: Cytochrome P450 3A4/5 ELISA Kit
SKU: DEIA-XYA519
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Cultured cells

Species Reactivity

Human

Detection Method

ELISA

Intended Use

The Cytochrome P450 3A4/5 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor target protein Cytochrome P450 3A4/5 and expression profile in cells. The kit can be used for measuring the relative amounts of Cytochrome P450 3A4/5 proteins in cultured cells as well as screening for the effects that various treatments, inhibitors (i.e. siRNA or chemicals), or activators have on Cytochrome P450 3A4/5.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate 1 Plate
2. 10x TBS 30 ml (10x) 1 month at 4°C
3. Quenching Buffer 24 ml (1x) 1 month at 4°C
4. Blocking Buffer 50 ml (1x) 1 month at 4°C
5. 15x Wash Buffer 60 ml (15x) 1 month at 4°C
6. 100x Anti-Cytochrome P450 3A4/5 Antibody 60 μl (100x) 1 month at 4°C
7. 100x Anti-GAPDH Antibody 60 μl (100x) 1 month at 4°C
8. HRP-Conjugated Anti-Rabbit IgG Antibody 6 ml (1x) 1 month at 4°C
9. HRP-Conjugated Anti-Mouse IgG Antibody 6 ml (1x) 1 month at 4°C
10. Primary Antibody Diluent 12 ml (1x) 1 month at 4°C
11. Ready to Use Substrate 12 ml (1x) 1 month at 4°C
12. Stop Solution 12 ml (1x) 1 month at 4°C
13. Crystal Violet Solution 6 ml (1x) 1 month at 4°C
14. SDS Solution 24 ml (1x) 1 month at 4°C
15. Adhesive Plate Seals 2 Seals 1 month at 4°C

Storage

Storage: 4°C
Expiration: 6 months from receipt

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Predictive pharmacogenetic biomarkers for breast cancer recurrence prevention by simvastatin

ACTA ONCOLOGICA

Authors: Ahern, Thomas P.; Damkier, Per; Feddersen, Soren; Kjaersgaard, Anders; Lash, Timothy L.; Hamilton-Dutoit, Stephen; Lythjohan, Cathrine Bredal; Ejlertsen, Bent; Christiansen, Peer M.; Cronin-Fenton, Deirdre P.

Abstract

Background: Statins treat hyperlipidemia and prevent cardiovascular morbidity and mortality. Evidence suggests that they also have anti-neoplastic activity. Several studies show a reduced rate of breast cancer recurrence among lipophilic statin users (e.g., simvastatin), motivating calls for clinical trials of statins in breast cancer patients. We measured the impact of genetic variation in statin-metabolizing enzymes and drug transporters on the recurrence rate in simvastatin-treated breast cancer patients. Methods: We conducted a nested case-control study among Danish women diagnosed with non-metastatic, invasive breast cancer between 2004-2010 who had filled >= 1 prescription for simvastatin after diagnosis. Cases were all breast cancer recurrences from the source population; one control was matched to each case on cancer stage, estrogen receptor and hormone therapy status, calendar period of diagnosis, and duration of simvastatin exposure. We genotyped variants in simvastatin-metabolizing enzymes (CYP3A4/rs35599367 and CYP3A5/rs776746) and drug transporters (ABCB1/rs2032582 and SLCO1B1/rs4149056), and estimated their association with recurrence with logistic regression models. Results: We observed protective (though imprecisely-measured) associations between variants in genes encoding drug transporters (ABCB1 and SLCO1B1) and simvastatin-metabolizing enzymes (CYP3A4 and CYP3A5) and breast cancer recurrence in simvastatin-treated women. For example, carrying two variant alleles in ABCB1 was associated with a 31% lower rate of recurrence (multivariable OR = 0.69, 95% CI: 0.31, 1.5). Conclusion: Our study provides weak evidence to support the use of genetic variation in ABCB1, SLCO1B1, CYP3A4, and CYP3A5 as biomarkers of breast tumor response to simvastatin. Validation of these findings within adjuvant clinical trials is encouraged.

High Doses of Delta(9)-Tetrahydrocannabinol Might Impair Irinotecan Chemotherapy: A Review of Potentially Harmful Interactions

CLINICAL DRUG INVESTIGATION

Authors: Kopjar, Nevenka; Fuchs, Nino; Karaconji, Irena Brcic; Zunec, Suzana; Katic, Anja; Kozina, Goran; Vrdoljak, Ana Lucic

Abstract

This review proposes the hypothesis that the effectiveness of irinotecan chemotherapy might be impaired by high doses of concomitantly administered Delta(9)-tetrahydrocannabinol (THC). The most important features shared by irinotecan and THC, which might represent sources of potentially harmful interactions are: first-pass hepatic metabolism mediated by cytochrome P450 (CYP) enzyme CYP3A4; glucuronidation mediated by uridine diphosphate glycosyltransferase (UGT) enzymes, isoforms 1A1 and 1A9; transport of parent compounds and their metabolites via canalicular ATP-binding cassette (ABC) transporters ABCB1 and ABCG2; enterohepatic recirculation of both parent compounds, which leads to an extended duration of their pharmacological effects; possible competition for binding to albumin; butyrylcholinesterase (BChE) inhibition by THC, which might impair the conversion of parent irinotecan into the SN-38 metabolite; mutual effects on mitochondrial dysfunction and induction of oxidative stress; potentiation of hepatotoxicity; potentiation of genotoxicity and cytogenetic effects leading to genome instability; possible neurotoxicity; and effects on bilirubin. The controversies associated with the use of highly concentrated THC preparations with irinotecan chemotherapy are also discussed. Despite all of the limitations, the body of evidence provided here could be considered relevant for human-risk assessments and calls for concern in cases when irinotecan chemotherapy is accompanied by preparations rich in THC.