CYP2C9 Double Nickase Plasmid (h): sc-403593-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYP2C9 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- CYP2C9 Double Nickase Plasmid (h) and CYP2C9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CYP2C9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP2C9 Double Nickase Plasmid (h) | sc-403593-NIC | 20 µg | $410.00 | |||
CYP2C9 Double Nickase Plasmid (h2) | sc-403593-NIC-2 | 20 µg | $410.00 |
CYP2C9 encodes a heme-thiolate cytochrome P450 monooxygenase that catalyzes oxidative biotransformation of diverse xenobiotics and endogenous substrates in the endoplasmic reticulum. As part of Phase I metabolism, CYP2C9 contributes to redox-dependent electron transfer via NADPH–cytochrome P450 reductase, shaping cellular exposure to reactive intermediates and downstream conjugation pathways. Genetic polymorphisms and altered hepatic expression of CYP2C9 are linked to interindividual variability in drug clearance and susceptibility to adverse drug reactions, making it a key locus in pharmacogenomics. Dysregulated CYP2C9 activity is also studied in the context of liver injury mechanisms and pathway-level remodeling of detoxification networks.
CYP2C9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CYP2C9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CYP2C9. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt CYP2C9 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of CYP2C9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.