2. Immunology/Inflammation Neuronal Signaling GPCR/G Protein Apoptosis
  3. FLAP Opioid Receptor Apoptosis STING
  4. SC13

SC13 is an orally active, selective Flap structure-specific endonuclease 1 (FEN1) inhibitor and mu opioid receptor (MOR) activator. SC13 impairs DNA damage repair and induces apoptosis in cancer cells. SC13 activates cGAS-STING signaling, increases chemokine secretion, and promotes CAR-T cell infiltration at solid tumour sites. SC13 can be used for the research of solid tumours and pain.

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SC13

SC13 Chemical Structure

CAS No. : 2839142-69-5

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SC13 Related Antibodies

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1 Publications Citing Use of MCE SC13

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μ Opioid Receptor/MOR κ Opioid Receptor/KOR δ Opioid Receptor/DOR NOP Receptor/ORL1

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Description

SC13 is an orally active, selective Flap structure-specific endonuclease 1 (FEN1) inhibitor and mu opioid receptor (MOR) activator. SC13 impairs DNA damage repair and induces apoptosis in cancer cells. SC13 activates cGAS-STING signaling, increases chemokine secretion, and promotes CAR-T cell infiltration at solid tumour sites. SC13 can be used for the research of solid tumours and pain[1][2].

IC50 & Target[2]

μ Opioid Receptor/MOR

 

In Vitro

SC13 (20 μM; 48 h) induces DNA double-strand break accumulation and cytoplasmic dsDNA leakage in HeLa, MCF-7, and SKOV-3 human cancer cells[1].
SC13 (20 μM; 48 h) activates the cGAS-STING pathway and increases chemokine (CCL5, CXCL10) and IFN-β expression in HeLa, MCF-7, and SKOV-3 human cancer cells, dependent on STING signalling[1].
SC13 (20 μM; 48 h) induces HeLa, MCF-7, and SKOV-3 cells to secrete chemokines that promote MSLN CAR-T cell migration via a TBK1-dependent mechanism[1].
SC13 (20 μM; 48 h) induces mild DNA damage but does not impair proliferation, CAR expression, or cytotoxic function of MSLN CAR-T cells[1].
SC13 potently inhibits cAMP production in human mu-opioid receptor-expressing HEK-T cells with an EC50 of 7.25 nM and maximum efficacy[2].
SC13 recruits β-arrestin2 in human mu-opioid receptor-expressing HTLA cells with low potency (EC50 = 11000 nM) and moderate efficacy[2].
SC13 acts as a partial agonist for Gi-1 G-protein activation in human mu-opioid receptor-expressing cells, with high selectivity for MOR over DOR and KOR[2].

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

SC13 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: HeLa, MCF-7, SKOV-3 human cancer cell lines
Concentration: 20 μM
Incubation Time: 48 h
Result: Upregulated γ-H2AX (a marker of DNA double-strand breaks) in HeLa, MCF-7, and SKOV-3 cells.
Increased cytoplasmic dsDNA leakage in these cell lines.

Real Time qPCR[1]

Cell Line: HeLa, MCF-7, SKOV-3 human cancer cell lines
Concentration: 20 μM
Incubation Time: 48 h
Result: Activated the cGAS-STING pathway and increased chemokine (CCL5, CXCL10) and IFN-β expression, dependent on STING signalling.

Cell Migration Assay [1]

Cell Line: MSLN CAR-T cells, HeLa, MCF-7, SKOV-3 human cancer cell lines
Concentration: 20 μM
Incubation Time: 48 h
Result: Significantly increased the number of migrating MSLN CAR-T cells compared to medium from vehicle-treated tumour cells; this effect was blocked by pre-treatment of tumour cells with the TBK1 inhibitor Amlexanox.
Increased secretion of CCL5 and CXCL10 in the supernatant of SC13-treated tumour cells.
In Vivo

SC13 (5 mg/kg; i.p.; every other day for 32 days) enhances MSLN CAR-T cell-mediated anti-tumour efficacy in HeLa xenografts, reducing tumour weight by ~60%, increasing intratumoural CD8+ T-cell infiltration by ~168%, and elevating intratumoural CCL5 and CXCL10 levels, with no observed organ toxicity[1].
SC13 (1-15 mg/kg; s.c. or p.o.; single dose; 10 mg/kg) produces MOR-dependent antinociception in mice with an ED50 of 3.05 mg/kg s.c., and maintains efficacy via oral administration[2].
SC13 (15 mg/kg; s.c.; daily; 2 days) does not induce reward or dysphoria in Mus musculus[2].
SC13 (15 mg/kg; s.c.; single dose) does not inhibit gastrointestinal transit in mice[2].
SC13 (45 mg/kg; s.c.; single dose) does not induce respiratory depression or hyperlocomotion in mice[2].

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

Animal Model: B-NDG (6 weeks old; injected 5 × 106 HeLa cells subcutaneously into the mice)[1]
Dosage: 5 mg/kg
Administration: i.p.; every other day for 32 days
Result: Reduced mean tumour weight to ~0.2 g compared to ~0.5 g in CAR-T alone group.
Increased intratumoural CD8+ T-cell infiltration to 18.65% of tumour-infiltrating cells compared to 6.95% in CAR-T alone group.
Increased CD8 signal intensity ~4-fold compared to CAR-T alone group.
Elevated CCL5 fluorescence intensity ~3-fold compared to CAR-T alone group.
Elevated CXCL10 fluorescence intensity ~2-fold compared to CAR-T alone group.
Caused no significant change in mouse body weight.
Showed no exacerbated organ damage to heart, liver, spleen, lung, or kidney.
Animal Model: C57BL/6J mice (20-32 g)[2]
Dosage: 1 mg/kg; 3 mg/kg; 10 mg/kg; 15 mg/kg
Administration: s.c. or p.o.; single dose
Result: Produced dose-dependent antinociception.
Reached a maximum of ~30% MPE at 20 minutes post-administration with 1 mg/kg s.c..
Reached ~30% MPE at 20 minutes post-administration with 3 mg/kg s.c..
Reached 100% MPE at 20 minutes post-administration with 10 mg/kg s.c..
Achieved an ED50 of 3.05 mg/kg s.c. for antinociception.
Showed significantly reduced antinociception in MOR knockout mice, but remained intact in KOR knockout and DOR knockout mice.
Reached a peak of 87% MPE at 30 minutes post-administration with 10 mg/kg p.o..
Animal Model: C57BL/6J mice (20-32 g)[2]
Dosage: 15 mg/kg
Administration: s.c.; daily; 2 days
Result: Produced no significant conditioned place preference or aversion.
Showed no statistically significant difference in time spent in the drug-paired compartment compared to pre-conditioning.
Animal Model: C57BL/6J mice (20-32 g)[2]
Dosage: 15 mg/kg
Administration: s.c.; single dose
Result: Had no significant effect on gastrointestinal transit.
Resulted in charcoal traveling 30.8 cm, a value indistinguishable from saline-treated mice.
Animal Model: C57BL/6J mice (20-32 g)[2]
Dosage: 45 mg/kg
Administration: s.c.; single dose
Result: Showed no statistically significant respiratory depression compared to vehicle.
Had breath rate comparable to vehicle/saline controls at all time points except 180 and 200 minutes, where it showed a slight increase.
Produced no significant hyperlocomotion.
Had ambulation distance indistinguishable from vehicle/saline controls at all time points.
Molecular Weight

450.53

Formula

C26H30N2O5
CAS No.
SMILES

O=C(OC)/C([C@@H](C[C@]12[H])[C@H](CC)CN1CC[C@@]3(O)C2=NC4=C3C(C5=COC=C5)=CC=C4)=C/OC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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SC13 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

SC132839142-69-5SC 13SC-13FLAPOpioid ReceptorApoptosisSTING5-lipoxygenase-activating protein5-LO activating proteinStimulator of Interferon GenesTMEM173MITAERISMPYSSKOV-3FEN1antinociceptionCAR-T cellMORcGAS-STING signalingapoptosisDNA damage repairMCF-7HeLaInhibitorinhibitorinhibit

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