1. Membrane Transporter/Ion Channel
    Autophagy
  2. CFTR
    Autophagy
  3. KM11060

KM11060 

Cat. No.: HY-19970 Purity: 99.80%
Handling Instructions

KM11060 is a corrector of the F508 deletion (F508del)-cystic fibrosis transmembrane conductance regulator (CFTR) trafficking defect. KM11060 can be used for the research of F508del-CFTR processing defect and development of cystic fibrosis therapeutics.

For research use only. We do not sell to patients.

KM11060 Chemical Structure

KM11060 Chemical Structure

CAS No. : 774549-97-2

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 77 In-stock
Estimated Time of Arrival: December 31
10 mg USD 70 In-stock
Estimated Time of Arrival: December 31
25 mg USD 150 In-stock
Estimated Time of Arrival: December 31
50 mg USD 270 In-stock
Estimated Time of Arrival: December 31
100 mg USD 490 In-stock
Estimated Time of Arrival: December 31
200 mg   Get quote  
500 mg   Get quote  

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Customer Review

Based on 4 publication(s) in Google Scholar

Top Publications Citing Use of Products

Publications Citing Use of MCE KM11060

    KM11060 purchased from MCE. Usage Cited in: Patent. US20150328217A1.

    CFTR correctors (Compounds A to F) promote the rescue of R98H mutant of alpha-sarcoglycan in HEK293 cell model. Alpha-sarcoglycan (α-SG) protein level has been determined by western blot (a representative experiment is shown in the top panel) on total protein content purified from cells expressing the R98H mutant treated with either CFTR correctors (compound A, B, C, D, E and F as indicated), MG132 (proteasome inhibitor) used as positive control, or correctors vehicle (DMSO) used as negative con

    KM11060 purchased from MCE. Usage Cited in: Patent. US9987256B2.

    CFTR correctors (Compounds A to F(KM11060)) promote the rescue of R98H mutant of alpha-sarcoglycan in HEK293 cell model.
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    Description

    KM11060 is a corrector of the F508 deletion (F508del)-cystic fibrosis transmembrane conductance regulator (CFTR) trafficking defect. KM11060 can be used for the research of F508del-CFTR processing defect and development of cystic fibrosis therapeutics[1].

    In Vitro

    Small-molecule correctors such as KM11060 may serve as useful pharmacological tools in studies of the F508del-CFTR processing defect and in the development of cystic fibrosis therapeutics. KM11060 rescues F508del-CFTR trafficking in cultured cells and native epithelial tissues. KM11060 partially corrects F508del-CFTR processing and increases surface expression to 75% of that observed in cells incubated at low temperature. Up to 50% of the F508del-CFTR in cells treated with KM11060 was complex-glycosylated, indicating passage through the Golgi. KM11060 as a promising compound for further development of CF therapeutics. [1]

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    In Vivo

    In LPS-induced acute lung inflammation, blockade of PSGL-1 (P-selectin glycoprotein ligand-1) or P-selectin, antagonism of PAF by WEB2086, or correction of mutated CFTR trafficking by KM11060 could significantly increase plasma lipoxin A4 levels in F508del relevant to wildtype mice. [2]

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight

    422.33

    Formula

    C₁₉H₁₇Cl₂N₃O₂S

    CAS No.

    774549-97-2

    SMILES

    O=S(N1CCN(C2=CC=NC3=CC(Cl)=CC=C23)CC1)(C4=CC=C(Cl)C=C4)=O

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    References
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    Keywords:

    KM11060KM 11060KM-11060CFTRAutophagyCystic fibrosis transmembrane conductance regulatorInhibitorinhibitorinhibit

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