QC-308
QC-308 is a HO-1/HO-2 inhibitor, with an IC50 of 0.27 μM against rat HO-1 and an IC50 of 0.46 μM against rat HO-2. QC-308 inhibits the activities of rat HO-1 and HO-2 in carbon monoxide generation assays using spleen and brain microsomes, respectively. QC-308 also exhibits senolytic activity, reducing the survival rate of adipogenic progenitor cells in skeletal muscle fibers of senescent mice and human skeletal muscle myoblasts. QC-308 is applicable for senescence-related research.
For research use only. We do not sell to patients.
- CAS No.: 1353712-58-9
- Formula: C19H18N2O
- Molecular Weight:290.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
HO-1 0.27 μM (IC50) |
HO-2 0.46 μM (IC50) |
In Vitro
QC-308 potently inhibits HO-1 activity in rat spleen microsomes with an IC50 of 0.27 μM, and inhibits HO-2 activity in rat brain microsomes with an IC50 of 0.46 μM[1].
QC-308 binds to truncated recombinant hHO‑1 and hHO‑2, alters the heme environment of both proteins, and inhibits heme degradation in a dose-dependent manner; the hHO‑2 system retains 87.2% of intact heme, while the hHO‑1 system reduces the initial heme degradation rate to 9.8% of the control group and retains 71.6% of intact heme simultaneously[1].
QC-308 binds to truncated recombinant hHO-1 through a "double-prong" mode, occupying two independent hydrophobic pockets and coordinating with heme iron, thereby forming a stable inhibitor-enzyme complex[1].
QC-308 (1.00×10‑9-1.00×10‑3 M; 5 days) exhibits a senescence-dependent slight reduction in viability in senescent primary mouse FAPs; it does not show a senescence-specific decrease in viability in senescent primary mouse SCs; and it induces a senescence-dependent decline in viability in senescent human skeletal myoblasts[2].
QC-308 (1-500 μM; 72 h) does not exhibit senolytic activity in senescent mouse skin fibroblasts and human lung fibroblasts (IMR-90 cells) [2].
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:primary mouse fibro-adipogenic progenitors (FAPs)
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Concentration:1×10‑9, 1×10‑8, 1×10‑7, 1×10‑6, 1×10‑5, 1×10‑4 M
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Incubation Time:5 days
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Result:Slightly but significantly decreased the viability of senescent FAPs in a senescence-dependent manner, with minimal effect on non-senescent FAPs.
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Cell Line:primary mouse skeletal muscle satellite cells (SCs)
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Concentration:1×10‑9, 1×10‑8, 1×10‑7, 1×10‑6, 1×10‑5, 1×10‑4 M
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Incubation Time:5 days
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Result:Showed no difference in killing between senescent and non-senescent SCs.
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Cell Line:human skeletal muscle myoblasts (HSMMs)
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Concentration:1×10‑9, 1×10‑8, 1×10‑7, 1×10‑6, 1×10‑5, 1×10‑4, 1×10‑3 M
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Incubation Time:3 days
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Result:Significantly decreased the viability of senescent HSMMs in a senescence-dependent manner, with minimal effect on non-senescent HSMMs.
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Cell Line:mouse dermal fibroblasts (mDFs)
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Concentration:10, 50, 100, 200, 500 μM
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Incubation Time:72 h
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Result:Was ineffective at inducing senolysis in mDFs, showing no significant difference in viability between senescent and non-senescent cells.
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Cell Line:human lung fibroblasts (IMR-90 cells)
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Concentration:1, 10, 100 μM
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Incubation Time:72 h
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Result:Was ineffective at inducing senolysis in IMR-90 cells, showing no significant difference in viability between senescent and non-senescent cells.
Chemical Information
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CAS No. 1353712-58-9
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Molecular Weight 290.36
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Formula C19H18N2O
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SMILES
O=C(CC(C1=CC=CC=C1)C2=CC=CC=C2)CN3C=NC=C3
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Senescence-associated β-galactosidase staining
Senescence-associated β-galactosidase staining detects β-galactosidase activity that is histochemically visible at pH 6. 0 in senescent cells, where X-gal cleavage produces an insoluble blue precipitate observable by bright-field microscopy. This activity reflects increased lysosomal β-galactosidase/lysosomal mass rather than a senescence-essential enzyme, because GLB1 depletion or genetic lysosomal β-galactosidase deficiency can abolish SA-β-gal staining while cells still undergo senescence. SA-β-gal was originally reported in senescent but not presenescent fibroblasts and keratinocytes, absent from quiescent fibroblasts and terminally differentiated keratinocytes, and increased with donor age in human skin samples. Because SA-β-gal can also appear in some non-senescent or tissue-specific contexts, interpretation should be paired with experimental controls and, when possible, independent senescence markers.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)