1. PROTAC Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR MAPK/ERK Pathway Stem Cell/Wnt
  2. Molecular Glues FGFR PI3K Akt p38 MAPK ERK
  3. LC-MG-10

LC-MG-10 is a selective molecular glue degrader targeting FGFR2, with a DC50 of 230.2 nM in KATO III cells. LC-MG-10 induces proteasomal degradation of FGFR2 via a covalent molecular glue mechanism. LC-MG-10 inhibits cancer cell proliferation. LC-MG-10 suppresses FGFR2-mediated PI3K/AKT and MAPK/ERK signaling pathways. LC-MG-10 can be used in studies related to gastric cancer.

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LC-MG-10

LC-MG-10 Chemical Structure

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Description

LC-MG-10 is a selective molecular glue degrader targeting FGFR2, with a DC50 of 230.2 nM in KATO III cells. LC-MG-10 induces proteasomal degradation of FGFR2 via a covalent molecular glue mechanism. LC-MG-10 inhibits cancer cell proliferation. LC-MG-10 suppresses FGFR2-mediated PI3K/AKT and MAPK/ERK signaling pathways. LC-MG-10 can be used in studies related to gastric cancer[1].

IC50 & Target[1]

FGFR2

230.2 nM (DC50)

In Vitro

LC-MG-10 (0-10000 nM; 12 h) potently induces dose-dependent degradation of FGFR2 in KATO III gastric cancer cells, with a DC50 of 230.2 nM[1].
LC-MG-10 (0-1000 nM; 12 h) inhibits FGFR2-mediated PI3K/AKT and MAPK/ERK signaling pathways in KATO III gastric cancer cells following 12 h of treatment at concentrations of 300 nM and 1000 nM[1].
LC-MG-10 (1 μM; 0-12 h) induces the internalization of FGFR2 from the plasma membrane into intracellular vesicles in KATO III gastric cancer cells[1].
LC-MG-10 (1 μM; 0 h-8 h) induces time-dependent degradation of FGFR2 in KATO III gastric cancer cells[1].
LC-MG-10 (96 h) potently inhibits the proliferation of KATO III gastric cancer cells, with an IC50 value of 49.13 nM[1].
Degradation of FGFR2 in KATO III gastric cancer cells induced by LC-MG-10 (200 nM) depends on the ubiquitin-proteasome system[1].
LC-MG-10 (1 μM; 1 h) binds to the ATP-binding pocket of FGFR2 to mediate its degradation, whereas pre-treatment with the parent inhibitor Infigratinib (HY-13311) blocks this activity in KATO III gastric cancer cells[1].

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

Western Blot Analysis[1]

Cell Line: KATO III cells
Concentration: 0, 300, 1000 nM
Incubation Time: 12 h
Result: Abrogated both the PI3K/AKT and MAPK/ERK signaling cascades, as evidenced by the markedly diminished phosphorylation of the primary docking protein FRS2α (Tyr436), as well as
PLCγ (Tyr783), SHP2 (Tyr524), AKT (Ser473), ERK1/2, and the downstream terminal kinase RSK1 (Thr573).

Immunofluorescence[1]

Cell Line: KATO III cells
Concentration: 1 μM
Incubation Time: 0, 6, 12 h
Result: Triggered the rapid relocalization of FGFR2 from the plasma membrane into intracellular vesicular compartments.

Western Blot Analysis[1]

Cell Line: KATO III cells
Concentration: 1 μM
Incubation Time: 0, 1, 2, 4, 8 h
Result: Induced time-dependent degradation of FGFR2 in KATO III gastric cancer cells, with detectable depletion starting at 4 hours and maximal clearance by 8 hours of treatment with 1 μM.
Molecular Weight

720.60

Formula

C35H35Cl2N7O6

SMILES

O=C(NC1=C(Cl)C(OC)=CC(OC)=C1Cl)N(C2=NC=NC(NC3=CC=C(N4CCN(C(/C=C/C(C5=CC=C(OC)C=C5)=O)=O)CC4)C=C3)=C2)C

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Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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Product Name:
LC-MG-10
Cat. No.:
HY-184322
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