crispr

Brefeldin A (Cyanein) belongs to the class of macrolide antibiotics and is an ATPase inhibitor (IC₅₀=0.2 μM). Brefeldin A can induce tumor cell differentiation and apoptosis, and also possesses autophagy inhibitory activity.

Zidovudine (ZDV) is a synthetic dideoxynucleoside. After intracellular phosphorylation to its active metabolite, zidovudine inhibits DNA polymerase, resulting in the inhibition of DNA replication and cell death. This agent also decreases levels of available pyrimidines.

SCR7 pyrazine (SCR7) enhances CRISPR-Cas9-mediated homology-directed repair (HDR) efficiency in vitro up to 19-fold. Inhibits nonhomologous end-joining (NHEJ).

BRD0539 is a cell-permeable spCas9 inhibitor that blocks the binding of spCas9 to DNA and inhibits Streptococcus pyogenes Cas9 (SpCas9).

Nocodazole (Oncodazole) is a reversible inhibitor of microtubule polymerization and an inhibitor of Bcr-Abl. Nocodazole has antitumor activity, blocks the cell cycle and induces apoptosis.

SCR7, a specific DNA Ligase IV inhibitor, blocks nonhomologous end-joining (NHEJ).

NU7441 (KU-57788 (NU7441)) is a highly effective and specific DNA-PK inhibitor (IC₅₀: 14 nM).

L755507 is an effective, selective agonist of β3-AR(IC₅₀=35 nM).

BRD7586 is a cell-permeable small molecule inhibitor of SpCas9 that enhances SpCas9 specificity.

RS-1 is a RAD51 activator. RS-1 also increases CRISPR/Cas9-mediated knock-in efficiencies.

BRD20322 is a novel potent inhibitor of spCas9 that disrupts spCas9-DNA binding and exerts dose and temporal control of spCas9 in human cell lines. It reduces off-target DNA editing events, enhancing the precision and safety of CRISPR-Cas9 gene editing.

(iso)-BRD20322 is an isomer of BRD20322, a novel potent inhibitor of spCas9 that disrupts the binding of spCas9 to DNA and reduces non-specific DNA editing events, thereby improving the safety and accuracy of the CRISPR-Cas9 gene editing system.

CEM114 is a potent chemical compound known as a chemical epigenetic modifier (CEM). It functions by employing CRISPR-Cas9 systems to harness endogenous chromatin machinery, thereby exerting its epigenetic modifying effects.

Mca-VDQVDGW-Lys(Dnp)-NH2, a fluorogenic substrate specific to caspase-7, facilitates the quantification of caspase-7 activity.

Degrader of MTH1 fusion proteins for use within the aTAG system. Comprises a ligand selective for MTH1, a linker and the cereblon-binding ligand Thalidomide . Induces highly potent and selective degradation of fusion proteins after a 4 h incubation (DC50 = 0.27 nM; Dmax = 92.1%). Cell-permeable. Suitable for in vitro and in vivo applications. Mouse DMPK properties are provided in the supplementary file (see below). (MTH1 can be expressed as a fusion with a target protein of interest using genome engineering techniques via CRISPR-mediated locus-specific knock-in - see protocol for more information.) 0

Degrader of MTH1 fusion proteins for use within the aTAG system. Comprises a ligand selective for MTH1, a linker and the cereblon-binding ligand Thalidomide . Induces highly potent and selective degradation of fusion proteins after a 4 h incubation (DC50 = 0.34 nM; Dmax = 93.14%). Cell-permeable. Suitable for in vitro and in vivo applications. Mouse DMPK properties are provided in the supplementary file (see below). (MTH1 can be expressed as a fusion with a target protein of interest using genome engineering techniques via CRISPR-mediated locus-specific knock-in - see protocol for more information.) 0

Degrader targeting mutant FKBP12F36V fusion proteins. Comprises a ligand selective for F36V single-point mutated FKBP12, a linker and a von Hippel-Lindau (VHL)-binding ligand. Induces potent and selective degradation of FKBP12F36V fusion proteins in vitro and in vivo. Selectively degrades FKBP12F36V-EWS/FLI fusion proteins and inhibits cell proliferation in FKBP12F36V-EWS/FLI-expressing Ewing sarcoma cells. Hydrochloride salt (Cat.No. 7374) available; suitable for in vivo use. Negative control dTAGV-1-NEG (Cat. No. 6915) also available. FKBP12F36V can be expressed as a fusion with a target protein of interest using genome engineering techniques, via transgene expression or CRISPR-mediated locus-specific knock-in. Custom knock-in cell lines for the dTAG and aTAG platforms are available from our sister brand R&D Systems. Email TPD@bio-techne.com to enquire. Plasmid vectors for the lentiviral expression and CRISPR-mediated knock-in of FKBP12F36V are available from Addgene.

SF2523 is a highly selective and potent inhibitor (SF2523) with improved physicochemical properties, excellent aqueous solubility, and biological efficacy. It is typically used in genome editing [CRISPR/Cas Solution] technology and can effectively enhance the efficiency of this process.

Cas9-IN-3 is a potent inhibitor of Cas9 with an IC₅₀ of 28 μM. The CRISPR/Cas systems have revolutionized gene editing in several species [1].

ZA3-Ep10, a zwitterionic lipid, is utilized in the formulation of lipid nanoparticles for RNA delivery in vivo and non-viral CRISPR/Cas gene editing applications.

N1,N3,N5-Tris(4-dodecylhexadecyl)benzene-1,3,5-tricarboxamide is an analogue of TT3 . TT3 is an ionizable lipid material utilized for the delivery of mRNA.

TT3 is an ionizable lipid-like material used for the delivery of mRNA and CRISPR/Cas9 [1] [2].

Peptide A5K acetate (INF7-A5K-TAT acetate) is an amphiphilic peptide derived from the HA2-TAT fusion scaffold, designed to facilitate macromolecular transport in genome editing. Peptide A5K acetate non-covalently binds to CRISPR RNP (ribonucleoprotein complex) and delivers it into cells such as primary human T cells, B cells, and NK cells, enabling low-toxicity, multi-target, highly efficient, and precise genome editing.

9A1P9 is a multi-tailed ionizable cationic lipid featuring multiple hydrophobic chains and a protonatable headgroup. Under acidic conditions, 9A1P9 enhances electrostatic interactions with nucleic acids, promotes endosomal escape, and improves intracellular mRNA delivery efficiency. 9A1P9 is commonly used in the construction of lipid nanoparticle (LNP) systems and in delivery mechanism studies.