Cat. No.: HY-183390

Scopadulciol

Scopadulciol is an orally effective β-catenin degrader, HSV-TK activator and proton pump inhibitor. By inducing β-catenin degradation, Scopadulciol downregulates the expression of downstream target genes such as cyclin D1, c-myc, and survivin; it also upregulates DR4/DR5 and downregulates Bcl-2, thereby exerting cytotoxicity and inducing apoptosis in cancer cells. Scopadulciol enhances the tumor-killing and bystander effects of prodrugs via activating HSV-TK, and can inactivate HSV-1. It shows synergistic antiviral effects when combined with Acyclovir (HY-17422) or Ganciclovir (HY-13637), with no cytotoxicity as a single agent. Scopadulciol can be applied in research related to bladder cancer, cervical cancer, glioblastoma, and digestive system cancers.

For research use only. We do not sell to patients.

CAS No.: 136565-26-9
Formula: C₂₇H₃₆O₄
Molecular Weight:424.57

Storage:

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

Scopadulciol Chemical Structure

CAS No.: 136565-26-9

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
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Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[4]

Bcl-2

HSV-1

All PROTACs Isoforms :

All Bcl-2 Family Isoforms :

All HSV Isoforms :

In Vitro

Scopadulciol (50-200 nM; 24 h) inhibits luciferase activity in both STF/293 and FOP-transfected HEK293 cells in a concentration-dependent manner, with non-specific inhibition of TOP activity at 50, 100, and 200 nM over 24 h^[1].
Scopadulciol (125-500 nM; 24-72 h) exhibits time-dependent cytotoxicity against human gastrointestinal cancer cell lines (SW480, HCT116, DLD1, AGS, RKO) and non-cancer HEK293 cells, with the lowest IC₅₀ of 70 nM observed in AGS cells after 72 h incubation^[1].
Scopadulciol (150-300 nM; 24 h) induces G0/G1 cell cycle arrest in RKO human colon cancer cells and dose-dependent sub-G1 accumulation (apoptosis) in AGS human gastric adenocarcinoma cells after 24 h incubation at 150 and 300 nM^[1].
Scopadulciol (100-400 nM; 24 h) reduces β-catenin levels and inhibits its nuclear localization in a concentration-dependent manner in AGS human gastric adenocarcinoma cells after 24 h incubation at 100, 200, and 400 nM, via a GSK3β-independent mechanism^[1].
Scopadulciol (400 nM; 24 h) induces proteasome-dependent β-catenin degradation in AGS human gastric adenocarcinoma cells at 400 nM over 24 h, an effect blocked by pretreatment with 10 μM MG132 or 10 μM Epoxomicin (HY-13821), and not mediated by caspases or calpains^[1].
Scopadulciol (50-200 nM; 24-48 h) induces p53-dependent β-catenin degradation and cytotoxicity in AGS human gastric adenocarcinoma cells; it increases p53 levels at 50, 100, and 200 nM over 24 h, and its β-catenin-degrading and cytotoxic effects are blocked by Pifithrin-α (HY-123076) ^[1].
Scopadulciol (0.2-4 μM, 100-400 nM; 24 h) specifically inhibits TCF/β-catenin transcriptional activity at 0.2, 2, and 4 μM and downregulates Wnt/β-catenin target proteins (cyclin D1, c-myc, survivin) in a concentration-dependent manner in AGS human gastric adenocarcinoma cells after 24 h incubation^[1].
Scopadulciol (50-200 nM; 12-24 h) sensitizes TRAIL-resistant AGS human gastric adenocarcinoma cells to TRAIL-induced apoptosis, with combined treatment of 200 nM scopadulciol and 100 ng/mL TRAIL reducing AGS viability to 7% after 24 h and inducing apoptosis in 27.7% of cells after 12 h, while being less toxic to non-cancer HEK293 cells^[1].
Scopadulciol (50-200 nM; 24 h) upregulates DR4 and DR5 levels and downregulates Bcl-2 levels in a concentration-dependent manner in AGS human gastric adenocarcinoma cells after 24 h incubation at 50, 100, and 200 nM^[1].
Scopadulciol (1-100 μM) mildly inhibits hog gastric H⁺,K⁺-ATPase, with 45% inhibition observed at 100 μM^[3].
Scopadulciol (0.04 µM; 5 days) potently enhances the cytotoxicity of ACV and GCV against HSV-TK-expressing HEp-2-HSTK, EJ-1-HSTK, HeLa 229-HSTK, and YKG-1-HSTK cells, with no effect on parental TK⁻ cells^[2].
Scopadulciol (0.04-0.1 µM; 7 days) significantly enhances the bystander effect of ACV and GCV in mixed HeLa-TK⁺/HeLa-TK⁻ cell cultures, with greater potentiation at the higher 0.1 µM concentration^[2].
Scopadulciol (0.04 μM) significantly enhances the cytotoxicity of ACV and GCV in HSV-tk-expressing human cancer cell lines (HEp-2-HSTK, EJ-1-HSTK, HeLa 229-HSTK, TKG-1-HSTK) without affecting wild-type cancer cells or showing independent cytotoxicity^[4].
Scopadulciol (0.04 µM; 90 min at 37°C) selectively stimulates HSV-TK activity in HeLa-TK⁺ cell lysates without affecting cellular kinase activity in HeLa-TK⁻ cell lysates^[2].
Scopadulciol (0.02-0.04 µM) significantly increases intracellular GCV-TP levels in HeLa-TK+ cells treated with 100 µM GCV^[2].
Scopadulciol (0.01-1 µM; 5 h at 37°C) does not affect the activity of cellular kinases responsible for converting ACV-MP to ACV-TP in HeLa-TK⁻ cell lysates^[2].
Scopadulciol (6 h) reduces HSV-1 infectivity in a concentration-dependent manner by inactivating the virus, with no inhibitory effect on HSV-1 or HeLa cell-derived DNA polymerase^[4].
Scopadulciol selectively activates HSV-TK in HeLa-TK⁺ cells, with no effect on TK activity in HeLa-TK⁻ cells^[4].
Scopadulciol (0.05-0.1 μM) acts synergistically with Acyclovir to inhibit HSV-1 replication in HeLa cells by increasing intracellular ACV-TP concentrations, with no enhanced cytotoxicity^[4].

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

Cell Cytotoxicity Assay^[1]

Cell Line:

human gastrointestinal cancer cell lines (SW480, HCT116, DLD1, AGS, RKO), non-cancer HEK293 cells
Concentration:

125, 250 and 500 nM
Incubation Time:

24 h, 48 h, 72 h
Result:

Reduced cell viability in all tested cell lines in a time-dependent manner.
Exhibited an IC₅₀ of 359 nM for RKO cells after 24 h, with IC₅₀ >500 nM for SW480, HCT116, DLD1, AGS, and HEK293 cells.
Exhibited an IC₅₀ of 101 nM for AGS cells, 374 nM for RKO cells, and 227 nM for HEK293 cells after 48 h, with IC₅₀ >500 nM for SW480, HCT116, and DLD1 cells.
Exhibited an IC₅₀ of 296 nM for SW480 cells, 70 nM for AGS cells, 479 nM for RKO cells, and 181 nM for HEK293 cells after 72 h, with IC₅₀ >500 nM for HCT116 and DLD1 cells.
Increased RKO cell viability after 48 h.
Continued to decrease AGS cell viability over 72 h.

Cell Cycle Analysis^[1]

Cell Line:

RKO human colon cancer cells, AGS human gastric adenocarcinoma cells
Concentration:

150 and 300 nM
Incubation Time:

24 h
Result:

Increased the G0/G1 population in RKO cells in a concentration-dependent manner (from 46.9% in controls to 67.5% at 300 nM) with no significant change in the sub-G1 population.
Caused a concentration-dependent increase in the sub-G1 population in AGS cells (from 3.7% in controls to 27.3% at 300 nM), indicating induction of apoptosis.

Western Blot Analysis^[1]

Cell Line:

AGS human gastric adenocarcinoma cells
Concentration:

100, 200 and 400 nM
Incubation Time:

24 h
Result:

Decreased β-catenin levels in whole cell, cytoplasmic, and nuclear fractions in a concentration-dependent manner.
Reduced nuclear β-catenin levels, indicating inhibition of β-catenin nuclear localization.
Decreased levels of GSK3β and phosphorylated β-catenin, suggesting β-catenin degradation was independent of GSK3β.

Western Blot Analysis^[1]

Cell Line:

AGS human gastric adenocarcinoma cells
Concentration:

400 nM (scopadulciol); 10 μM (MG132, epoxomicin)
Incubation Time:

24 h (scopadulciol); 1 h (MG132, epoxomicin pretreatment)
Result:

Had its induced β-catenin degradation abolished by pretreatment with MG132 or epoxomicin.
Showed no significant effect on β-catenin degradation when cells were pretreated with pan-caspase inhibitor z-VAD-fmk or calpain inhibitor calpastatin.
Saw no significant effect on β-catenin levels from MG132 or epoxomicin alone.

Western Blot Analysis^[1]

Cell Line:

AGS human gastric adenocarcinoma cells
Concentration:

50, 100 and 200 nM; 20 μM, 100 ng/mL (Pifithrin-α)
Incubation Time:

24 h, 48 h
Result:

Increased p53 levels in a concentration-dependent manner.
Had its induced β-catenin degradation abolished by pretreatment with pifithrin-α.
Had its cytotoxic activity abrogated by pifithrin-α in AGS cells.

Cell Cytotoxicity Assay^[1]

Cell Line:

AGS human gastric adenocarcinoma cells, non-cancer HEK293 cells
Concentration:

50, 100 and 200 nM; 100 ng/mL (TRAIL (HY-P78528))
Incubation Time:

12 h, 24 h
Result:

Reduced AGS cell viability to 70% at 200 nM alone after 24 h.
Reduced AGS cell viability to 7% when combined with 100 ng/mL TRAIL after 24 h.
Induced apoptosis in 27.7% of AGS cells when combined with 100 ng/mL TRAIL after 12 h, compared to 5.7% with TRAIL alone and 3.5% with scopadulciol alone.
Caused less viability reduction in HEK293 cells than in AGS cells when combined with TRAIL.
Saw TRAIL alone (100 ng/mL) reduce AGS viability to 86%.

Western Blot Analysis^[1]

Cell Line:

AGS human gastric adenocarcinoma cells
Concentration:

50, 100 and 200 nM
Incubation Time:

24 h
Result:

Increased protein levels of death receptors DR4 and DR5 in a concentration-dependent manner.
Decreased levels of antiapoptotic protein Bcl-2 in a concentration-dependent manner.

Cell Proliferation Assay^[2]

Cell Line:

HSV-TK-expressing (TK+) human cancer cell lines (HEp-2-HSTK, EJ-1-HSTK, HeLa 229-HSTK, YKG-1-HSTK), parental TK− cancer cell lines (HEp-2, EJ-1, HeLa 229, YKG-1)
Concentration:

0.04 µM (co-administered with Acyclovir (ACV) (HY-17422) or Ganciclovir (GCV) (HY-13637))
Incubation Time:

5 days
Result:

Showed no toxicity to any tested cell line and did not augment ACV or GCV toxicity in TK− cells.
Reduced ACV IC₅₀ values to 4.0-23 µM (8-21-fold lower than ACV alone) in TK+ cell lines, with statistically significant reductions (p < 0.01 to p < 0.001 compared to prodrug alone).
Reduced GCV IC₅₀ values to 0.15-1.2 µM (5-41-fold lower than GCV alone) in TK+ cell lines, with statistically significant reductions (p < 0.01 to p < 0.001 compared to prodrug alone).

In Vivo

Scopadulciol (1 mg per day; p.o.; three times daily, once every 8 h; for 14 consecutive days; i.p.; three times daily, once every 8 h; for 14 consecutive days; i.p.; twice daily, once every 12 h; for 14 consecutive days) significantly enhances the antitumor efficacy of Acyclovir (HY-17422) and Ganciclovir (HY-13637) in nude mice bearing HeLa tumors with 100% HSV-TK expression: when combined with Ganciclovir, it reduces tumor volume by 1.8 to 6.3 folds, and when combined with Acyclovir, it produces effects comparable to or better than those of Ganciclovir monotherapy^[2].
Scopadulciol (1 mg per day; oral administration; three times daily; 14 days) alone fails to inhibit the growth of HSV-TK-expressing HeLa tumors in nude mice, but it significantly enhances the antitumor efficacy when co-administered with Acyclovir or Ganciclovir^[4].
Scopadulciol (1 mg/day; oral administration; three times daily; 14 days) enhances the antitumor efficacy of Acyclovir against HSV-TK⁻/HSV-TK⁺ mixed HeLa tumors in nude mice, which supports the bystander effect^[4].
Scopadulciol (0.33 mg per mouse; p.o.; single administration; i.p.; single administration) significantly increases the bioavailability of Acyclovir and Ganciclovir in nude mice; when administered via intraperitoneal injection, the AUC_0-t of Ganciclovir can be increased up to 2.76-fold^[2].

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

Animal Model:

Mice (5-week-old female ddY athymic nude mice) were subcutaneously inoculated in the back with 5 × 10⁶ HeLa cells (containing 100%, 10%, or 0% HSV-TK⁺ cells). The experiment was initiated 10-13 days later, when the tumor volume had grown to >100 mm³.
^[2]
Dosage:

1 mg/day
Administration:

p.o.; three times a day every 8 hours; 14 days; i.p.; three times a day every 8 hours; 14 days; i.p.; twice a day every 12 hours; 14 days
Result:

Showed a non-significant tendency to suppress tumor growth over 6 weeks when administered orally alone.
Significantly enhanced oral ACV's antitumor effect from day 14 to day 42 compared to ACV monotherapy when combined with oral 4 mg/day ACV.
Reduced tumor volume more effectively than ACV alone, with tumor volume remaining lower throughout the observation period when combined with oral 4 mg/day ACV.
Significantly reduced tumor growth from day 14 to day 42 compared to no-drug control when administered intraperitoneally alone.
Prevented tumor growth entirely during the 6-week observation period, with significantly greater antitumor effects from day 23 onward compared to ACV monotherapy when combined with i.p. 2.5 mg/day ACV.
Produced the most marked tumor volume reduction over 42 days, with significant differences compared to GCV monotherapy from day 14 to day 42 when combined with i.p. 2.5 mg/day GCV.
Reduced tumor volume to 130% of baseline (vs. 234% for GCV alone) when combined with i.p. 0.25 mg/day GCV.
Reduced tumor volume to 28% of baseline (vs. 176% for GCV alone) when combined with i.p. 1 mg/day GCV.
Reduced tumor volume to 20% of baseline (vs. 113% for GCV alone) when combined with i.p. 2.5 mg/day GCV.
Reduced tumor volume to 64% of baseline (vs. 289% for ACV alone) when combined with i.p. 1 mg/day ACV.
Reduced tumor volume to 43% of baseline (vs. 128% for ACV alone) when combined with i.p. 2.5 mg/day ACV.
Reduced tumor volume to 96% of baseline (vs. 195% for ACV alone) when combined with oral 4 mg/day ACV.

Animal Model:

ddY athymic nude mice (5-week-old female)^[2]
Dosage:

0.33 mg/mouse
Administration:

p.o.; single dose; i.p.; single dose
Result:

Significantly increased plasma acyclovir concentrations at 1 hour (p < 0.05), 2 hours (p < 0.01), and 4 hours (p < 0.05) post-administration, resulting in an AUC₀→∞ that was ~1.27-fold higher than acyclovir monotherapy when co-administered orally with oral acyclovir.
Significantly increased plasma acyclovir concentrations at 0.5 hours and 1 hour (p < 0.05) post-administration, resulting in an AUC₀→∞ that was ~2.41-fold higher than acyclovir monotherapy when co-administered intraperitoneally with i.p. acyclovir.
Significantly increased plasma ganciclovir concentrations at 0.5 hours, 1 hour, and 4 hours (p < 0.01) post-administration, resulting in an AUC₀→∞ that was ~2.76-fold higher than ganciclovir monotherapy when co-administered intraperitoneally with i.p. ganciclovir.

Animal Model:

Mice were subcutaneously inoculated with HeLa-TK⁺ cells^[4]
Dosage:

1 mg/day (monotherapy; combination with ACV); 1 mg/day (combination with GCV)
Administration:

p.o.; three times daily; duration of study (monotherapy, combination with ACV); i.p.; daily; duration of study (combination with GCV)
Result:

Did not significantly reduce tumor volume compared to control group.
Significantly suppressed tumor growth compared to control group and ACV monotherapy group.
Significantly suppressed tumor growth compared to control group and GCV monotherapy group.

Animal Model:

Nude mice were subcutaneously inoculated with a mixture of HeLa-TK⁺ and HeLa-TK⁻ cells at a ratio of 1:9^[4]
Dosage:

1 mg/day
Administration:

p.o.; three times daily; duration of study
Result:

Significantly suppressed tumor growth compared to control group and ACV monotherapy group.

Chemical Information

CAS No. 136565-26-9
Molecular Weight 424.57
Formula C₂₇H₃₆O₄
SMILES

C[C@@]12[C@]34[C@@](CC([C@](C3)(CC4)C)=O)([H])C[C@H]([C@@]1([H])[C@@](C)(CCC2)CO)OC(C5=CC=CC=C5)=O
Structure Classification
- Terpenoids
- Triterpenes
Initial Source
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

Handling Instructions (2659 KB)

References

[1]. Fuentes RG, et al. Scopadulciol, Isolated from Scoparia dulcis, Induces β-Catenin Degradation and Overcomes Tumor Necrosis Factor-Related Apoptosis Ligand Resistance in AGS Human Gastric Adenocarcinoma Cells. Journal of natural products. 2015 Apr 24;78(4):864-72. [Content Brief]

[2]. Hayashi K, et al. The role of a HSV thymidine kinase stimulating substance, scopadulciol, in improving the efficacy of cancer gene therapy. The journal of gene medicine. 2006 Aug;8(8):1056-67. [Content Brief]

[3]. Hayashi T, et al. Scopadulciol, an inhibitor of gastric H+, K(+)-ATPase from Scoparia dulcis, and its structure-activity relationships. Journal of natural products. 1991;54(3):802-9. [Content Brief]

[4]. Hayashi T, et al. [Studies on evaluation of natural products for antiviral effects and their applications]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan. 2008 Jan;128(1):61-79. [Content Brief]

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Scopadulciol

All PROTACs Isoforms

All Bcl-2 Family Isoforms

All HSV Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

Scopadulciol Related Classifications

HY-183390 Related Classifications