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Fig. 1 · Structure
Cat. No.
A11002
CAS No.
781661-94-7
Formula
C20H19BrN4O3
Mol. Weight
443.3

Documents & Downloads

Sepantronium Bromide (YM155)

Survivin Inhibitor

YM155 is a novel small molecule survivin suppressant with an IC50 of 0.54 nM for the inhibition of survivin promoter activity.

In Stock

Publications for Sepantronium Bromide

13 publications citing this product

  1. Atieh Pourbagheri-Sigaroodi, .et al. , Iran J Allergy Asthma Immunol, 2024, 23(6):699-726 PMID: 39985496
  2. Bopei Cui, .et al. , Signal Transduct Target Ther, 2023, Sep 25;8(1):366 PMID: 37743418
  3. Ali Nasrollahzadeh, .et al. , Biochim Biophys Acta Mol Cell Res, 2021, Jun 26;1868(10):119087 PMID: 34182011
  4. Chia-Hui Huang, .et al. , Toxicol Appl Pharmacol, 2020, Apr 17;397:115013 PMID: 32305283
  5. Turner TH, .et al. , Sci Rep, 2020, Jan 30;10(1):1493 PMID: 32001757
  6. Chiou JT, .et al. , Toxicol Appl Pharmacol, 2019, Dec 16;387:114857 PMID: 31837377
  7. Hamzehlou S, .et al. , Eur J Pharmacol, 2019, Nov 15;863:172705 PMID: 31574259
  8. Momeny M, .et al. , Cell Oncol (Dordr), 2019, Apr 25 PMID: 31025257
  9. Yamamoto M, .et al. , Anticancer Res, 2019, Feb;39(2):609-617 PMID: 30711936
  10. Vázquez-Mellado MJ, .et al. , Oncol Rep, 2018, Nov 27 PMID: 30483799
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Biological Activity

Target & Activity

Target Activity Value
Survivin (HeLa-SURP-luc, CHO-SV40-luc cells) 0.54 nM

Cellular Effect

Cell Line Activity Value Description Reference
DU-145 EC50 13.8 nM Cytotoxicity against human DU145 cells by MTT assay [PMID: 28774426]
MDA-MB-435 IC50 > 1 μM Antiproliferative activity against human MDA-MB-435/LCC6MDR cells assessed as inhibition of cell growth incubated for 72 hrs by MTS assay [PMID: 34371464]
MDA-MB-435 IC50 2.4 μM Antiproliferative activity against human MDA-MB-435 cells assessed as inhibition of cell growth incubated for 72 hrs by MTS assay [PMID: 34371464]
PC-3 EC50 92 nM Cytotoxicity against human PC3 cells by MTT assay [PMID: 28774426]
Vero C1008 CC50 400 μM Cytotoxicity against African green monkey Vero E6 cells assessed as cell viability treated for 24 hrs by CCK8 assay [PMID: 35620927]

In Vitro Studies

In MDA468, HCC1143 and HCC1937 basal-like triple-negative breast cancer cells, YM155 combined with afatinib produced synergistic viability inhibition after 72 h at high effect levels (combination index <1 at fraction affected >0.75). These results describe the combination relative to the single-agent dose responses. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

YM155 and afatinib in three basal-like TNBC cell lines

Cell-based study · Human MDA468, HCC1143 and HCC1937 basal-like triple-negative breast cancer cell lines [1]

The single-agent dose responses were used as controls for combination analysis. After 72 h, the afatinib–YM155 combination was synergistic at high effect levels in all three cell lines. This is a combination result; it does not establish a direct molecular target or clinical benefit. Interaction behavior depends on effect level.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Combination effect on cell viabilityCombination index CI < 1 at Fa > 0.75[1]
Dose reduction relative to each single agent at a matched effectDose reduction index DRI > 1 for both drugs at Fa > 0.75[1]

Literature-Reported Treatment Conditions

Treatment concentration
Seven doses of each drug, singly and in all pairwise dose combinations; constant-ratio analysis used afatinib:YM155 = 50:1. Exact seven-dose grid not transcribed.
Exposure duration
72 h
Method
CellTiter-Glo luminescent viability assay, normalized to vehicle controls
Vehicle
DMSO; Figure 7 uses viability as percent of vehicle. Exact vehicle percentage for this cell-line validation is not specified in the read methods.
Co-treatment
Afatinib plus YM155; each drug alone and vehicle were comparator conditions.
Reported limits
Salt form and batch analytical identity are not specified. The exact seven-dose grid is not tabulated in the read main-text cell-line methods; no concentrations were inferred from plotted points.
Methods and source locations

Compound reported in the paper: YM155; Compound label in the paper: YM155 as reported; salt unspecified

Results concern the material described as YM155. No salt conversion, stereochemical inference, or validation of the current A11002 lot is made.

Figure 7a–e and caption; Methods: Breast cancer cell lines, Cell viability assays, In vitro drug screening studies, Multiple-dose drug combination studies; Results combination section

Combination effect on cell viability: CellTiter-Glo viability; Chou–Talalay analysis with CompuSyn; constant afatinib:YM155 dose ratio 50:1. Two independent experiments, each in triplicate; SD shown. — Figure 7a–c and caption; Results: Afatinib and YM155 are synergistically cytotoxic across TNBC PDXs; Methods: Cell viability assays and Multiple-dose drug combination studies

Dose reduction relative to each single agent at a matched effect: CompuSyn analysis of the same combination experiment; DRI represents calculated dose reduction at equal effect, not an administered dose. — Figure 7d–e and caption; Methods: Multiple-dose drug combination studies

In Vivo Studies

In an HCI01 mammary xenograft model in NSG mice (n = 3 per group), YM155 alone and combined with afatinib reduced tumor growth and terminal tumor weight versus untreated controls. The combination did not significantly improve tumor-growth control over YM155 alone. No considerable body-weight changes were observed during this small experiment. [1]

YM155 alone and with afatinib in an HCI01 mammary PDX model

Animal study · HCI01 human basal-like TNBC mammary PDX in female NSG mice; four groups of 3 mice [1]

YM155 alone and with afatinib reduced tumor growth and terminal tumor weight relative to untreated mice. Adding afatinib did not significantly improve tumor-growth control over YM155 alone. No considerable body-weight change or observable toxicity was reported; this small study does not establish comprehensive safety.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Tumor growth measured as tumor area (length × width)Between-group comparison YM155 and afatinib + YM155 reduced growth versus untreated; no significant difference between YM155 alone and the combination.[1]
Terminal excised tumor weight and monitored mouse body weightQualitative group comparisons Tumor weight reduced with YM155 alone and combination versus untreated; afatinib alone versus untreated was not significant. No considerable body-weight changes observed.[1]
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
UntreatedUntreated reference groupLargest tumors; comparator for treatment effects.[1]
Afatinib alone
25 mg/kg		Untreated miceReduced tumor growth versus untreated, but terminal tumor weight was not significantly different from untreated.[1]
YM155 alone
5 mg/kg, as reported		Untreated mice; afatinib alone; combinationReduced tumor growth and terminal tumor weight versus untreated. No significant tumor-growth difference versus combination.[1]
Afatinib + YM155
Afatinib 25 mg/kg; YM155 5 mg/kg, as reported		Untreated and each single agentReduced growth versus untreated and afatinib alone, without significant improvement over YM155 alone. Terminal tumor weight reduced versus untreated.[1]
Untreated
Model: HCI01 human basal-like TNBC mammary PDX in female NSG mice; n = 3 mice per group
Treatment course: Observed alongside treatment groups
Reported limits: YM155 is reported as 5 mg/kg over a 7-day continuous infusion regimen; the source does not explicitly label this as mg/kg/day. Salt form and lot not specified.
Afatinib alone
Model: HCI01 human basal-like TNBC mammary PDX in female NSG mice; n = 3 mice per group
Route: Oral gavage
Frequency: Daily
Treatment course: 7 days
Vehicle: 1% methylcellulose + 0.1% Tween-80
Reported limits: YM155 is reported as 5 mg/kg over a 7-day continuous infusion regimen; the source does not explicitly label this as mg/kg/day. Salt form and lot not specified.
YM155 alone
Model: HCI01 human basal-like TNBC mammary PDX in female NSG mice; n = 3 mice per group
Route: Subcutaneous infusion via Alzet pump
Frequency: Continuous
Treatment course: 7 days
Vehicle: Saline
Reported limits: YM155 is reported as 5 mg/kg over a 7-day continuous infusion regimen; the source does not explicitly label this as mg/kg/day. Salt form and lot not specified.
Afatinib + YM155
Model: HCI01 human basal-like TNBC mammary PDX in female NSG mice; n = 3 mice per group
Route: Afatinib oral gavage; YM155 subcutaneous infusion
Frequency: Afatinib daily; YM155 continuous
Treatment course: 7 days
Vehicle: Afatinib: 1% methylcellulose + 0.1% Tween-80; YM155: saline
Reported limits: YM155 is reported as 5 mg/kg over a 7-day continuous infusion regimen; the source does not explicitly label this as mg/kg/day. Salt form and lot not specified.
Methods and source locations

Compound reported in the paper: YM155; Compound label in the paper: YM155 as reported; Adooq Bioscience material

Results concern the material described as YM155. No salt conversion, stereochemical inference, or validation of the current A11002 lot is made.

Figure 8a–d and caption; Results animal-validation section; Methods: Breast cancer PDX models, In vivo PDX drug treatment studies and Statistical analyses

Tumor growth measured as tumor area (length × width): Serial caliper measurements; n = 3 mice/group; SD shown. Source uses unpaired Student t tests and p < 0.05 as significance criterion; exact SI p-values not extracted. — Figure 8a; Results animal-validation section; Methods: In vivo PDX drug treatment studies and Statistical analyses

Terminal excised tumor weight and monitored mouse body weight: Ex vivo tumor weighing and serial mouse weights; n = 3 mice/group, SD shown. No exact bar heights extracted. — Figure 8b–c and caption; Results animal-validation section

Untreated · Figure 8a–d and caption; Results: Afatinib and YM155 reduce PDX mammary tumor growth in vivo; Methods: In vivo PDX drug treatment studies

Afatinib alone · Figure 8a–d and caption; Results: Afatinib and YM155 reduce PDX mammary tumor growth in vivo; Methods: In vivo PDX drug treatment studies

YM155 alone · Figure 8a–d and caption; Results: Afatinib and YM155 reduce PDX mammary tumor growth in vivo; Methods: In vivo PDX drug treatment studies

Afatinib + YM155 · Figure 8a–d and caption; Results: Afatinib and YM155 reduce PDX mammary tumor growth in vivo; Methods: In vivo PDX drug treatment studies

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 781661-94-7
Applications Survivin Inhibitor
Formula C20H19BrN4O3
Molecular Weight 443.3
Synonyms YM155
SMILES
CC1=[N+](C2=C(N1CCOC)C(=O)C3=CC=CC=C3C2=O)CC4=NC=CN=C4.[Br-]

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 52 mg/mL (117.3 mM)
Water 85 mg/mL (191.75 mM)
Ethanol 6 mg/mL (13.53 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
Saline

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Tia H. Turner, Mohammad A. Alzubi, J. Chuck Harrell. Identification of synergistic drug combinations using breast cancer patient-derived xenografts Scientific Reports (2020). PMID: 32001757 DOI: 10.1038/s41598-020-58438-0 Source material

Publications

13 publications citing this product

  1. Atieh Pourbagheri-Sigaroodi, .et al. , Iran J Allergy Asthma Immunol, 2024, 23(6):699-726 PMID: 39985496
  2. Bopei Cui, .et al. , Signal Transduct Target Ther, 2023, Sep 25;8(1):366 PMID: 37743418
  3. Ali Nasrollahzadeh, .et al. , Biochim Biophys Acta Mol Cell Res, 2021, Jun 26;1868(10):119087 PMID: 34182011
  4. Chia-Hui Huang, .et al. , Toxicol Appl Pharmacol, 2020, Apr 17;397:115013 PMID: 32305283
  5. Turner TH, .et al. , Sci Rep, 2020, Jan 30;10(1):1493 PMID: 32001757
  6. Chiou JT, .et al. , Toxicol Appl Pharmacol, 2019, Dec 16;387:114857 PMID: 31837377
  7. Hamzehlou S, .et al. , Eur J Pharmacol, 2019, Nov 15;863:172705 PMID: 31574259
  8. Momeny M, .et al. , Cell Oncol (Dordr), 2019, Apr 25 PMID: 31025257
  9. Yamamoto M, .et al. , Anticancer Res, 2019, Feb;39(2):609-617 PMID: 30711936
  10. Vázquez-Mellado MJ, .et al. , Oncol Rep, 2018, Nov 27 PMID: 30483799
  11. MASAHIRO YAMAMOTO, .et al. , Anticancer Res, 2018, Dec 38 (12) 6699-6706 PMID: 30504379
  12. Ahn MR, .et al. , Drug Discov Ther, 2017, 11(6):300-306 PMID: 29332887
  13. MASAYA MINODA, .et al. , Int J Oncol, 2015, Sep; 47(3): 891-899 PMID: 26166250

Showing 10 of 13 publications

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