MG-Lin1
MG-Lin1 is a Lin28/Lin28A molecular glue degrader with a DC50 of approximately 0.7 μM. It induces Lin28 degradation via the ubiquitin-proteasome pathway by forming a ternary complex, thereby upregulating the levels of let-7 miRNA and reducing the expression of its downstream oncogenic targets KRAS and PDK1, and inhibiting cancer cell migration. MG-Lin1 can be used in studies of ovarian cancer and choriocarcinoma.
For research use only. We do not sell to patients.
- Formula: C23H18F3N5O
- Molecular Weight:437.42
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
Lin28 0.7 μM (DC50) |
Ras |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| PA-1 | EC50 |
0.1 μM
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50% reduction of normalized Renilla luciferase intensity in human PA-1 ovarian cancer cells via Lin28/let-7 luciferase reporter assay following 24 h incubation.
50% reduction of normalized Renilla luciferase intensity in human PA-1 ovarian cancer cells via Lin28/let-7 luciferase reporter assay following 24 h incubation.
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39575661 |
| PA-1 | DC50 |
0.7 μM
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Proteasome-dependent degradation of endogenous Lin28 protein in human PA-1 ovarian cancer cells measured via western blot following 48 h incubation.
Proteasome-dependent degradation of endogenous Lin28 protein in human PA-1 ovarian cancer cells measured via western blot following 48 h incubation.
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39575661 |
In Vitro
MG-Lin1 (0.1-100 μM; 24 h) potently enhances the activity of let-7 in PA-1 ovarian cancer cells, reducing the normalized luciferase intensity by 50% after 24 h of incubation at a concentration of 0.1 μM[1].
MG-Lin1 (0.01-10 μM; 48 h) induces proteasome-dependent degradation of Lin28 in PA-1 ovarian cancer cells, with a degradation rate of 66% after treatment at 1 μM for 48 h, and its DC50 is approximately 0.7 μM[1].
MG-Lin1 (1-10 μM; 48 h) significantly increases the abundance of let-7c miRNA in PA-1 ovarian cancer cells, with the abundance elevated by more than 2-fold after treatment at 10 μM for 48 h[1].
MG-Lin1 (10 μM; 48 h) reduces the mRNA levels of oncogenic KRAS and PDK1 in PA-1 ovarian cancer cells; after incubation at 10 μM for 48 h, the level of KRAS decreases to approximately 60% of that in the vehicle control group, and the level of PDK1 decreases to approximately 35% of that in the vehicle control group[1].
MG-Lin1 (10 μM; 72 h) reduces the migration capacity of PA-1 ovarian cancer cells by 55% after incubation at a concentration of 10 μM for 72 h[1].
MG-Lin1 (10 μM; 48 h) more effectively increases the abundance of let7-c in JAR cells compared with other tested degraders[1].
MG-Lin1 (1 μM; 24 h) reduces the mRNA expression levels of KRAS and PDK1 in PA1 cells[1].
MG-Lin1 (48 h) reduces the KRAS protein level in JAR cells to 66% of that in the vehicle control group[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:PA-1 ovarian cancer cells
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Concentration:0.01, 0.1, 1, 10 μM; 10 μM (with proteasome inhibitor co-treatment)
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Incubation Time:48 h
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Result:Reduced Lin28 protein levels in a dose-dependent manner, causing a 66% decrease at 1 μM, with a DC50 of approximately 0.7 μM.
Blocked Lin28 reduction when co-treated with proteasome inhibitors, confirming proteasome-mediated degradation.
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Cell Line:PA-1 ovarian cancer cells
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Concentration:1, 10 μM
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Incubation Time:48 h
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Result:Increased relative let-7c abundance significantly, with a greater than 2-fold increase observed at 10 μM.
Showed a more pronounced increase than a comparable PROTAC derivative at the same dose.
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Cell Line:PA-1 ovarian cancer cells
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Concentration:10 μM
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Incubation Time:48 h
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Result:Reduced relative KRAS mRNA abundance significantly to approximately 60% of vehicle control.
Reduced relative PDK1 mRNA abundance significantly to approximately 35% of vehicle control.
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Cell Line:PA-1 ovarian cancer cells
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Concentration:10 μM
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Incubation Time:72 h
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Result:Inhibited PA-1 cell migration significantly, reducing wound closure by 55% as measured by relative wound density compared to untreated cells.
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Cell Line:JAR cells
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Concentration:10 μM
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Incubation Time:48 h
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Result:Increased let7-c abundance to a level higher than vehicle control.
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Cell Line:PA1 cells
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Concentration:1 μM
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Incubation Time:24 h
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Result:Decreased KRAS mRNA levels relative to vehicle control.\nDecreased PDK1 mRNA levels relative to vehicle control.
Chemical Information
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Molecular Weight 437.42
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Formula C23H18F3N5O
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SMILES
CC1=NN=C2C=CC(C3=CC=CC(N(C)C(/C=C/C4=CC=C(C=C4)C(F)(F)F)=O)=C3)=NN12
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Scratch/Wound-Healing Migration Assay
The scratch/wound-healing migration assay measures collective migration of adherent cells into an experimentally created cell-free gap in a confluent monolayer. The readout is generated by imaging the gap immediately after scratching and at later time points, then quantifying reduction in wound area, wound width, or percentage closure as cells move into the denuded region. Gap closure reflects cell migration but may also include cell proliferation, so interpretation should distinguish migration-focused conditions from proliferation-driven closure when possible, such as by using short assay windows, serum-controlled conditions, cell counting, or proliferation controls reported in published protocols.
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Chemotaxis Gradient Chamber Assay 1
The chemotaxis gradient chamber assay is based on the principle of observing directional cell migration in response to a stable, linear or quasi-linear concentration gradient of a chemoattractant formed between two fluid reservoirs separated by a narrow observation chamber. Cells placed within the chamber respond to the gradient by polarized movement toward higher chemoattractant concentrations, allowing quantification of chemotactic behavior in real time under microscopy. The classic Zigmond chamber design enables simultaneous visualization of gradient formation and individual cell trajectories, making it suitable for studying leukocyte chemotaxis and other motile cell types in vitro.
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Under-Agarose Cell Migration Assay
The under-agarose cell migration assay is a classical in vitro chemotaxis method designed to evaluate directed cell movement through a semi-solid agarose matrix toward soluble chemoattractant gradients, enabling visualization and quantification of leukocyte or motile cell migration in a confined 2D-like environment. In this system, cells and chemoattractants are placed in separate wells cut into an agarose gel, allowing diffusion-driven gradient formation that guides directional migration, which is typically assessed by measuring migration distance, cell morphology changes, and accumulation toward the chemoattractant source. This assay has been widely used to study neutrophil and leukocyte chemotaxis as a simple alternative to filter-based migration systems and allows direct microscopic observation of migrating cells under near-physiological confinement conditions.
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Neural Crest/Neuronal Cell Migration Explant Assay
Neural crest (NC) and neuronal cell migration explant assays are in vitro systems in which neural tube-derived tissues are cultured to allow premigratory or newly emigrated neural crest cells to undergo epithelial-to-mesenchymal transition (EMT), migrate away from the explant, and form a measurable radial outgrowth that reflects migratory capacity and environmental responsiveness. These assays typically quantify migration by measuring the expansion of cell outgrowth from neural tube or neural plate border explants over time, often comparing early and later timepoints to derive a migration index such as a radius ratio, which reflects net cell dispersal from the explant core. Neural tube explant cultures preserve key aspects of neural crest behavior, including EMT, migration, and early differentiation, making them suitable for assessing intrinsic migratory ability and extrinsic cue dependence. However, studies emphasize that migratory outgrowth from neural tube explants may include non-n
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Transwell/Boyden Chamber Migration Assay
The Transwell/Boyden chamber migration assay measures cell movement through a porous membrane separating an upper and lower chamber, usually after a chemoattractant gradient is established by placing cells in the upper chamber and chemoattractant-containing medium in the lower chamber. The readout is generated by quantifying cells that traverse the membrane and appear on the lower membrane surface or in the lower chamber, depending on whether the cell type is adherent or non-adherent. This assay reflects chemotactic or haptotactic migration rather than matrix invasion unless an extracellular-matrix barrier is added to the membrane.
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3D Collagen/Hydrogel Matrix Migration Assay
The 3D collagen/hydrogel matrix migration assay is based on embedding cells within or on top of a fibrillar collagen type I-rich three-dimensional matrix to model in vivo-like extracellular matrix (ECM) architecture, enabling analysis of cell migration through a physically and biochemically relevant scaffold. In contrast to 2D migration systems, cells in 3D matrices interact with fibrillar collagen networks, requiring coordinated adhesion remodeling and proteolytic or non-proteolytic deformation mechanisms to move through confined spaces, thereby providing a more physiologically relevant readout of invasive and migratory behavior in tissue-like environments. Cell movement in 3D collagen matrices is typically quantified by tracking single-cell trajectories, invasion depth, or matrix penetration over time, reflecting combined effects of cytoskeletal dynamics, cell-ECM adhesion turnover, and ECM remodeling. These systems are widely used to study tumor cell invasion and stromal cell motili
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Cell-Exclusion Zone Migration Assay
The Cell-Exclusion Zone (CEZ) migration assay is an in vitro 2D cell migration method in which a defined cell-free area is created using removable physical barriers such as silicone stoppers, allowing cells to be seeded around the barrier and subsequently migrate into the cleared zone after barrier removal. This approach enables quantification of collective cell migration by monitoring repopulation of the initially cell-free region over time using microscopy-based imaging. Compared with scratch-based wound healing assays, barrier-based exclusion methods are designed to avoid mechanical damage to the extracellular matrix and reduce injury-induced effects on boundary cells, thereby improving interpretability of migration behavior in vitro. The assay readout is typically the progressive reduction in the cell-free area or the number of cells invading the exclusion zone, reflecting coordinated cell motility relevant to physiological processes such as wound healing, epithelial repair, and ca
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Chemotaxis Gradient Chamber Assay 2
Chemotaxis gradient chamber assays measure directional cell migration in response to a soluble chemical gradient by imaging cells as they move across a defined observation region; the readout is generated from time-lapse cell trajectories, displacement toward the gradient, forward migration index, trajectory plots, rose/polar plots, and statistical tests of non-random directionality. The Dunn chamber is a direct-viewing glass chamber in which cells migrate across a bridge between control and chemoattractant wells, allowing observation of cells in a linear concentration gradient; related direct-viewing formats include the Insall chamber, which supports defined unidirectional gradients and high numerical-aperture microscopy, and the μ-Slide Chemotaxis chamber, which supports long-term live-cell imaging and gradient characterization with fluorescent dye.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)