2. Search Result
Search Result
Results for "

Switch II

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

2

Click Chemistry

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-151523
    KRas G12R inhibitor 1

    		Ras Cancer
    KRas G12R inhibitor 1 (compound 3) is a KRas G12R selective covalent inhibitor that exploits the strong nucleophilicity of mutant cysteines and binds irreversibly in the Switch II region of K-Ras. KRas G12R inhibitor 1 can be used in cancer research .
    KRas G12R inhibitor 1
  • HY-126247
    BI-2852

    		Ras Cancer
    BI-2852 is a KRAS inhibitor for the switch I/II pocket (SI/II-pocket) by structure-based agent design with nanomolar affinity. BI-2852 is mechanistically distinct from covalent KRASG12C inhibitor (binds to switch II pocket) and binds ten-fold more strongly to active KRASG12D versus KRASwt (740 nM vs 7.5 μM). BI-2852 blocks GEF, GAP, and effector interactions with KRAS, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.
    BI-2852
  • HY-145928
    Divarasib
    1 Publications Verification

    GDC-6036

    		 Ras Cancer
    Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRAS G12C and irreversibly locks it in the inactive GDP-bound state.
    Divarasib
  • HY-126247B
    (R)-BI-2852

    		Others Cancer
    (R)-BI-2852 is the isomer of BI-2852 (HY-126247), and can be used as an experimental control. BI-2852 is a KRAS inhibitor for the switch I/II pocket (SI/II-pocket) by structure-based agent design with nanomolar affinity. BI-2852 is mechanistically distinct from covalent KRASG12C inhibitor (binds to switch II pocket) and binds ten-fold more strongly to active KRASG12D versus KRASwt (740 nM vs 7.5 μM). BI-2852 blocks GEF, GAP, and effector interactions with KRAS, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.
    (R)-BI-2852
  • HY-145928B
    Divarasib adipate

    GDC-6036 adipate

    		 Ras Cancer
    Divarasib (GDC-6036) adipate is an orally bioavailable, highly potent, and selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRAS G12C and irreversibly locks it in the inactive GDP-bound state .
    Divarasib adipate
  • HY-162112
    KRB-456

    		Ras Cancer
    KRB-456 is a small molecule that binds a dynamic allosteric binding pocket within the switch-I/II region of KRAS G12D. KRB-456 inhibits P-MEK, P-AKT, and P-S6 levels in vivo and inhibits the growth of cancer. KRB-456 can be used for the research of pancreatic cancer .
    KRB-456
  • HY-128522
    ARS-1323-alkyne

    		Ras Cancer
    ARS-1323-alkyne, a switch-II pocket (S-IIP) inhibitor, is a conformational specific chemical reporter of KRAS G12C nucleotide state in living cells . ARS-1323-alkyne is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    ARS-1323-alkyne
  • HY-124798
    Rheb inhibitor NR1
    1 Publications Verification

    		 mTOR Neurological Disease Inflammation/Immunology Cancer
    Rheb inhibitor NR1 is a Rheb inhibitor with an IC50 of 2.1 µM in the Rheb-IVK assay. Rheb inhibitor NR1 can directly bind Rheb in the switch II domain and selectively inhibit the activation of mechanistic target of rapamycin complex 1 (mTORC1). Rheb inhibitor NR1 inhibits the phosphorylation of mTORC1 driven T389pS6K1 and increases the phosphorylation of S473pAKT in a dose-dependent manner. Rheb inhibitor NR1 does not influence mTORC2 activity .
    (Rheb-IVK: Rheb-dependent mTORC1 kinase activity)
    Rheb inhibitor NR1
  • HY-134813
    MRTX1133
    3 Publications Verification

    		 Ras Cancer
    MRTX1133 is a noncovalent, potent, and selective KRAS G12D inhibitor. MRTX1133 optimally fills the switch II pocket and extends three substituents to favorably interact with the protein, resulting in an estimated KD against KRAS G12D of 0.2 pM. MRTX1133 prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRAS G12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells. MRTX1133 has single digit nanomolar activity in cellular assays and marked in vivo efficacy in tumor models harboring KRAS G12D mutations .
    MRTX1133

Inquiry Online

Your information is safe with us. * Required Fields.

Salutation

  

Country or Region *

Applicant Name *

 

Organization Name *

Department *

     

Email Address *

 

Product Name *

Cat. No.

  

Requested quantity *

Phone Number *

     

Remarks

Inquiry Online

Inquiry Information

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent: