Adhibin
Adhibin is a Myo9a/Myo9b class IX myosin inhibitor. Adhibin allosterically inhibits RhoGAP IX class myosin ATPase and motor activity (IC50 = 2.5 μM and 2.6 μM), downregulates RhoA/ROCK signaling, reduces active RhoA, phosphorylated myosin light chain, and actomyosin contractility, and disrupts actin polymerization, stress fibers, focal adhesions, and intercellular junctions. Adhibin shows low cytotoxicity, inhibits three-dimensional spheroid separation and migration, and delays organoid morphogenesis, and can be used in research on metastatic cancer.
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- Formule: C13H9Br2NO
- Masse moléculaire:355.02
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Activité biologique
Description
In Vitro
Adhibin (submicromolar concentration; overnight) reduces the attachment, spreading, and migration of A549, MLE-12, and B16-F1 cells, and at submicromolar concentrations causes loss of polarity and an approximately 2-fold reduction in migration in B16-F1 cells[1].
Adhibin (5-25 µM; 6 h/overnight) disrupts actin structures, focal adhesions, and pMLC2/NM2 cortical localization in B16-F1, A549, MLE-12, and NIH-3T3 cells[1].
Adhibin (25 µM; up to 10 h) reduces focal adhesion movement and accelerates focal adhesion disassembly in A549 cells[1].
Adhibin (10-25 µM; 18-24 h) reduces pMLC2 and phosphorylated MLCP in A549 and MLE-12 cells without altering total NM2A/B levels[1].
Adhibin (5 µM; 3 h) impairs the contractile ring pMLC2 and increases multinucleation in B16-F1 cells[1].
Adhibin (2-40 µM; 48 h) disrupts epithelial junctions in MLE-12 and Caco-2 cells, leading to mislocalization of ZO-1 and connexin-43 and loss of TEER[1].
Adhibin (5-25 µM; 72 h) completely blocks the 3D migration of NIH-3T3 spheroids at 10 µM and 25 µM concentrations, and inhibits spheroid assembly at higher concentrations[1].
Adhibin (25 µM; days 2-8) reduces budding and eccentricity in human colon organoids without affecting survival or proliferation markers[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:A549, MLE-12, and B16-F1 cell lines
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Concentration:25 µM (A549 and MLE-12 morphology); 5 µM and 10 µM (B16-F1); submicromolar (migration)
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Incubation Time:overnight; up to 6 h; 3 h (migration recordings); 1 h after seeding (spreading)
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Result:Caused separation of single cells and entire cell groups from confluent layers.
Cells gained height and circularity and showed reduced area.
Cells increasingly failed to attach and spread after seeding, maintaining high circularity, smaller area, and absence of flattening for hours.
B16-F1 cells showed polarity failures and whole-cell rounding without loss of viability; cells failed to establish stable matrix adhesions and maintained a rounded shape and size after settling.
Migration speed and mean square displacement declined dose-dependently, while randomness of migration remained unaffected.
Even submicromolar concentrations reduced migration by almost 2-fold.
MYO9B-silenced B16-F1 cells did not show the same pronounced shape and migration changes as control cells; single-cell migration was only slightly reduced.
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Cell Line:B16-F1, A549, MLE-12, and NIH-3T3 cells
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Concentration:5 µM, 10 µM, and 25 µM
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Incubation Time:6 h (lamellipodia effects); overnight (immunofluorescence)
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Result:At 5 µM, B16-F1 cells lost their polarized shape, developed multiple protrusive fronts, and displayed thinner lamellipodia within 6 h.
At 10 µM, cells shrank further and lamellipodia disappeared completely.
Microspikes retained length but lacked membrane embedment, extended beyond cortical edges, and showed reduced dynamics; the ratio between microspike length and lamellipodium width increased, and lamellipodia contained less F-actin.
Altered G-to-F-actin ratios and caused dose-dependent loss of stress fibres.
Active RhoA and Myo9b were mislocalized away from cortical sites and protruding fronts.
pMLC2 was lost from the rear cortex, stress fibres, and actin-rich cortical sites.
Myo9b was lost from filopodia tips and retraction fibres in NIH-3T3 cells.
Focal adhesion number and area decreased, with disappearance of paxillin, vinculin, and VASP from cortical and surface-associated structures; wash-out restored lamellipodia, stress fibres, and dynamic focal adhesions.
pMLC2 levels were reduced, and NM2A/B were lost from cortical and contractile structures without changes in total NM2A/B.
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Cell Line:NIH-3T3 mouse fibroblasts
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Concentration:10 µM and 25 µM (3D migration); 5 µM, 10 µM, and 25 µM (spheroid formation)
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Incubation Time:72 h
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Result:Completely abolished the ability of NIH-3T3 spheroids to separate from the 3D assembly and migrate at 10 µM and 25 µM.
Spheroid formation from single cells was retarded at 5 µM and 10 µM and completely suppressed at 25 µM.
Parmacokinetics
Chemical Information
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Masse moléculaire 355.02
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Formule C13H9Br2NO
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SMILES
BrC1=CC2=C(NC3=C2C=C(Br)C=C3CO)C=C1
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Adhibin Related Classifications
HY-170318 Related Classifications
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