2. Signaling Pathways
  3. Cell Cycle/DNA Damage
  4. CRISPR/Cas9

CRISPR/Cas9

CRISPR/Cas9

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The CRISPR/Cas9 system derived from bacterial adaptive immune systems is one of the most powerful genome editing technology. It is an RNA-guided genome editing tool that consists of a Cas9 nuclease and a single-guide RNA (sgRNA). By base-pairing with a DNA target sequence, the sgRNA enables Cas9 to recognize and cut a specific target DNA sequence, generating double strand breaks (DSBs) that trigger cell repair mechanisms and mutations at or near the DSBs sites. CRISPR/Cas9 technology has been studied extensively and its application has been expanded from the modification of the gene in cells to organisms. The potential role of CRISPR/Cas9 in gene therapy has made it to become one of the hottest pots in cancer treatment. Different concepts of CRISPR/Cas9-mediated cancer therapy, including tumor-related genes manipulating, tumor immunotherapy, tumor research modelling and anti-cancer drug resistance overcoming are established in various cancer types.

The greatest advantages of the CRISPR-Cas9 system are its simplicity and wide applicability in genome manipulations of almost all biological systems tested to date, including cell lines, stem cells, yeasts, worms, insects, rodents, and mammals. For a targetable DNA site, only a corresponding 20 nucleotide gRNA is needed to guide the CRISPR-Cas9 to cut the target DNA at the desired location. The repair of the broken DNA ends occurs either through NHEJ to generate indels, which has been used to generate random genomic mutations or through HDR in the presence of donor oligonucleotides or DNA fragments containing homologous sequences flanking the DSB sites to generate precise site-directed nucleotide or large gene replacements, leading to generation of targeted gene mutations or corrections.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-16592
    Brefeldin A
    		Activator 99.82%
    Brefeldin A (BFA) is a lactone antibiotic and a specific inhibitor of protein trafficking. Brefeldin A blocks the transport of secreted and membrane proteins from endoplasmic reticulum to Golgi apparatus. Brefeldin A is also an autophagy and mitophagy inhibitor. Brefeldin A is a CRISPR/Cas9 activator. Brefeldin A inhibits HSV-1 and has anti-cancer activity.
    Brefeldin A
  • HY-13520
    Nocodazole
    		Activator 99.59%
    Nocodazole (Oncodazole) is a rapidly-reversible inhibitor of microtubule. Nocodazole binds to β-tubulin and disrupts microtubule assembly/disassembly dynamics, which prevents mitosis and induces apoptosis in tumor cells. Nocodazole inhibits Bcr-Abl, and activates CRISPR/Cas9.
    Nocodazole
  • HY-11006
    KU-57788
    		Activator 99.95%
    KU-57788 (NU7441) is a highly potent and selective DNA-PK inhibitor with an IC50 of 14 nM. KU-57788 is an NHEJ pathway inhibitor. KU-57788 also inhibits PI3K and mTOR with IC50s of 5.0 and 1.7 μM, respectively.
    KU-57788
  • HY-107845
    SCR7 pyrazine
    		Agonist 99.96%
    SCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine is also a CRISPR/Cas9 enhancer which increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity.
    SCR7 pyrazine
  • HY-17413
    Zidovudine
    		Agonist 99.95%
    Zidovudine is a nucleoside reverse transcriptase inhibitor (NRTI), widely used to treat HIV infection. Zidovudine increases CRISPR/Cas9-mediated editing frequency.
    Zidovudine
  • HY-12742
    SCR7
    		Agonist 98.22%
    SCR7 is an unstable form that can be autocyclized into a stable form SCR7 pyrazine (HY-107845). SCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine is also a CRISPR/Cas9 enhancer which increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity.
    SCR7
  • HY-19793
    RS-1
    		Activator 98.95%
    RS-1 is a RAD51 activator, and also increases CRISPR/Cas9-mediated knock-in efficiencies.
    RS-1
  • HY-19334
    L755507
    		Agonist 98.33%
    L755507 is a potent, selective agonist of β3-AR with an IC50 of 35 nM. L755507 enhances the homology-directed repair (HDR)-mediated genome editing in CRISPR/Cas9 nickase system.
    L755507
  • HY-148730
    BRD7586
    		Inhibitor 99.03%
    BRD7586 is a cell-permeable small-molecule inhibitor of SpCas9. BRD7586 is the smallest known anti-CRISPR.
    BRD7586
  • HY-136251
    BRD0539
    		Inhibitor 98.03%
    BRD0539 is a cell-permeable and non-toxic inhibitor of CRISPR-Cas9. BRD0539 inhibits Streptococcus pyogenes Cas9 (SpCas9) (apparent IC50=22 μM) in an in vitro DNA cleavage assay.
    BRD0539
  • HY-145692
    Cas9-IN-3
    		Inhibitor 99.64%
    Cas9-IN-3 is a potent Cas9 inhibitor (IC50=28 μM). CRISPR/Cas systems have revolutionized gene editing in various species.
    Cas9-IN-3
  • HY-144118
    Cas9-IN-1
    		Inhibitor 98.22%
    Cas9-IN-1 is a potent Cas9 inhibitor (IC50=7.02 μM), acting by binding to apo-Cas9 to prevent Cas9:gRNA complex formation.
    Cas9-IN-1
  • HY-W590683
    9A1P9
    		≥99.0%
    9A1P9 is a multi-tail ionizable cationic phospholipid. 9A1P9 induces membrane destabilization. 9A1P9 can be used for CRISPR-Cas9 gene editing in mice.
    9A1P9
  • HY-164062
    LZCap AG(3'Acm) Cas9 mRNA
    The Cas9 protein, guided by sgRNA, induces DNA double-strand breaks (DSBs) at specific genomic locations, activating the cell's endogenous DNA repair mechanisms, non-homologous end joining (NHEJ), or homology-directed repair (HDR), for repairing the targeted DSBs, enabling genome DNA target recognition and cleavage. LZCap AG(3'Acm) Cas9 mRNA can be used together with purified sgRNA for CRISPR/Cas genome editing, where the expressed Cas9 protein acts in conjunction with sgRNA to perform cleavage.
    LZCap AG(3'Acm) Cas9 mRNA
  • HY-17413S1
    Zidovudine-13C,d3
    		Agonist
    Zidovudine-13C,d3 is the 13C- and deuterium labeled Zidovudine. Zidovudine is a nucleoside reverse transcriptase inhibitor (NRTI), widely used to treat HIV infection. Zidovudine increases CRISPR/Cas9-mediated editing frequency. Zidovudine-13C,d3 is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. It can also undergo strain-promoted alkyne-azide cycloaddition (SPAAC) reactions with molecules containing DBCO or BCN groups.
    Zidovudine-<sup>13</sup>C,d<sub>3</sub>
  • HY-136572
    CEM114
    CEM114 is an effective chemical epigenetic modifier (CEM) that recruits endogenous chromatin machinery through CRISPR-Cas9 systems.
    CEM114
  • HY-144119
    Cas9-IN-2
    		Inhibitor
    Cas9-IN-2 is a potent Cas9 inhibitor (IC50=246 μM), Cas9-IN-2 acts by binding to apo-Cas9 to prevent Cas9:gRNA complex formation, which can potentially be applied to modulate and control Cas9 activity in various applications.
    Cas9-IN-2
  • HY-P3476
    Mca-VDQVDGW-Lys(Dnp)-NH2
    Mca-VDQVDGW-Lys(Dnp)-NH2 is a fluorogenic substrate of caspase-7. Mca-VDQVDGW-K(Dnp)-NH2 can be used to quantify caspase-7 activity.
    Mca-VDQVDGW-Lys(Dnp)-NH2
  • HY-17413S
    Zidovudine-d3
    		Agonist
    Zidovudine-d3 is the deuterium labeled Zidovudine. Zidovudine is a nucleoside reverse transcriptase inhibitor (NRTI), widely used to treat HIV infection. Zidovudine increases CRISPR/Cas9-mediated editing frequency. Zidovudine-d3 is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. It can also undergo strain-promoted alkyne-azide cycloaddition (SPAAC) reactions with molecules containing DBCO or BCN groups.
    Zidovudine-d<sub>3</sub>
  • HY-E70220
    AsCas12a Nuclease
    AsCas12a Nuclease is a CRISPR nuclease, and can specifically cutting double-stranded DNA. AsCas12a Nuclease can be used for gene edited study.
    AsCas12a Nuclease
Cat. No. Product Name / Synonyms Application Reactivity