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Fig. 1 · Structure
Cat. No.
A12801
CAS No.
151823-14-2
Formula
C26H42N4O5
Mol. Weight
490.63

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Sapacitabine (CYC682)

Cat. No. A12801 CAS 151823-14-2
Sapacitabine is an orally bioavailable pyrimidine analogue prodrug with potential antineoplastic activity.

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Publications for Sapacitabine

1 publication citing this product

  1. Sally L George, .et al. , EBioMedicine, 2020, Aug 23;59:102971 PMID: 32846370
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Biological Activity

Bioactivity / Mechanism

Sapacitabine altered cell-cycle distribution in HCT116 cells. After 48 h at 6 μM, the G2/M fraction was 41%, compared with 8% in untreated cells; the S-phase fraction was 35% versus 5%. This cellular response does not by itself establish the underlying DNA strand-breaking chemistry. [1]

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

In Vitro Studies

In a neuroblastoma compound screen, sapacitabine produced greater sensitivity in ATRX-mutant isogenic cells than in ATRX-wild-type controls. The result was based on viability-curve AUC after five days and nominal, uncorrected screening criteria; it supports a model-specific research hypothesis. [2]

Cell-cycle redistribution after sapacitabine treatment

Cell-based study · HCT116 human colorectal cancer cells [1]

At 6 μM for 48 h, sapacitabine increased the S and G2/M fractions relative to untreated cells. CNDAC was a separately tested comparator at the same nominal concentration. This DNA-content assay does not directly demonstrate strand cleavage.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cells in G2/MPercentage of total cells Control 8%; sapacitabine 41%; CNDAC 36%[1]
Cells in S phase (described as late-S in Results)Percentage of total cells Control 5%; sapacitabine 35%; CNDAC 36%[1]

Literature-Reported Treatment Conditions

Treatment concentration
6 μM sapacitabine; 6 μM CNDAC comparator.
Exposure duration
48 h
Method
Propidium iodide DNA-content flow cytometry; untreated control.
Reported limits
Treatment vehicle and experiment-specific replicate count/error bars are not supplied for Figure 3; no error term inferred.
Methods and source locations

Compound reported in the paper: Sapacitabine; Compound label in the paper: CYC682 / CS-682

Compound-level literature evidence; no certificate, catalog-number or lot equivalence established for A12801.

Figure 3 and caption; Results: Effect of sapacitabine and CNDAC on cell cycle changes; Methods: Cell cycle analysis and apoptosis

Cells in G2/M: Printed Figure 3 bar labels, cross-checked against Results. — Figure 3 lower panels and Results: Effect of sapacitabine and CNDAC on cell cycle changes

Cells in S phase (described as late-S in Results): Printed Figure 3 bar labels; DNA-content flow cytometry. — Figure 3 lower panels; corresponding Results

ATRX-associated sensitivity in a neuroblastoma compound screen

Cell-based study · SKNSH and isogenic TP53-mutant p53(2) control cells versus TP53/ATRX-mutant derivatives A3, E1 and E6 [2]

Sapacitabine was a selective-sensitivity hit in screen 2: lower viability-curve AUC in the ATRX-mutant group. Selection required an uncorrected nominal p≤0.05 and an AUC difference >0.1. This is a genotype-associated screening result, not clinical validation or proof of a sapacitabine-specific molecular mechanism.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Relative sensitivity associated with ATRX mutationAUC-based screening hit Greater sensitivity in ATRX-mutant group; met nominal p≤0.05 and AUC-difference >0.1 criteria.[2]

Literature-Reported Treatment Conditions

Treatment concentration
Screen 2: eight dose levels, maximum 1 μM; exact sapacitabine series not extracted.
Exposure duration
5 days after compound addition.
Method
CellTiter-Glo viability and dose-response AUC; two independent screen replicates, triplicate wells per dose; mixed-effects analysis.
Vehicle
0.2% DMSO viability control; 2 μg/mL puromycin cell-death control.
Methods and source locations

Compound reported in the paper: Sapacitabine; Compound label in the paper: CYC682 / CS-682

Compound-level literature evidence; no certificate, catalog-number or lot equivalence established for A12801.

Sections 2.7 and 3.2; Figure 3b; Table S2 screen 2 compound list

Relative sensitivity associated with ATRX mutation: Qualitative Figure 3b placement and Results; no exact AUC or p value inferred from the plot. — Figure 3b; sections 2.7 and 3.2

In Vivo Studies

In an MV4-11 mouse xenograft study, oral sapacitabine combined with vorinostat reduced tumour growth more than the corresponding single agents. Day-14 mean tumour volumes were 245 and 107 mm³ for the 5 and 15 mg/kg sapacitabine combinations, respectively, versus 875 mm³ for vehicle. Single-agent effects were relatively minimal at the tested doses. No treatment-related deaths were reported. [3]

Sapacitabine plus vorinostat in an MV4-11 xenograft

Animal study · Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size [3]

Combination treatment reduced tumour growth more than the corresponding single agents. Statistical analysis used day 14 because some vehicle mice required euthanasia for tumour burden. Single agents had relatively minimal effects at these doses and reached the experimental endpoint by day 17. No treatment-related deaths were reported; this does not establish comprehensive absence of toxicity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Day-14 tumour growthMean tumour volume and tumour growth inhibition (TGI) Vehicle 875 mm³; sapacitabine 5 mg/kg + vorinostat 33 mg/kg: 245 mm³, TGI 92%; sapacitabine 15 mg/kg + vorinostat 33 mg/kg: 107 mm³, TGI 112%.[3]
Between-group tumour responseOne-way ANOVA P<0.00001[3]
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Vehicle controlComparator for active treatment armsDay-14 mean tumour volume 875 mm³; some mice euthanized for tumour burden >1000 mm³.[3]
Sapacitabine 5 mg/kgVehicleRelatively minimal single-agent effect; experimental endpoint reached by day 17.[3]
Sapacitabine 15 mg/kgVehicleRelatively minimal single-agent effect; experimental endpoint reached by day 17.[3]
Vorinostat single agent
33 mg/kg		VehicleRelatively minimal single-agent effect; experimental endpoint reached by day 17.[3]
Sapacitabine 5 mg/kg + vorinostat
Sapacitabine 5 mg/kg; vorinostat 33 mg/kg		Vehicle and corresponding single agentsDay 14: 245 mm³ mean tumour volume; TGI 92%.[3]
Sapacitabine 15 mg/kg + vorinostat
Sapacitabine 15 mg/kg; vorinostat 33 mg/kg		Vehicle and corresponding single agentsDay 14: 107 mm³ mean tumour volume; TGI 112%.[3]
Vehicle control
Model: Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size
Treatment course: Vehicle control; exact vehicle schedule not specified in adopted methods.
Vehicle: Sapacitabine vehicle reported as 2.5% dimethylacetate and 9.75% emulphor; vorinostat in 40% hydroxypropyl-β-cyclodextrin.
Reported limits: No exact arm-specific n beyond ≥6; no curve-derived values added.
Sapacitabine 5 mg/kg
Model: Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size
Route: Oral
Frequency: Once daily
Treatment course: 4 days, 3-day break, then another 4 days
Vehicle: 2.5% dimethylacetate and 9.75% emulphor (as reported)
Reported limits: No exact arm-specific n beyond ≥6; no curve-derived values added.
Sapacitabine 15 mg/kg
Model: Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size
Route: Oral
Frequency: Once daily
Treatment course: 4 days, 3-day break, then another 4 days
Vehicle: 2.5% dimethylacetate and 9.75% emulphor (as reported)
Reported limits: No exact arm-specific n beyond ≥6; no curve-derived values added.
Vorinostat single agent
Model: Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size
Route: Intraperitoneal
Frequency: Once daily
Treatment course: 12 consecutive days, starting one day after group assignment
Vehicle: 40% hydroxypropyl-β-cyclodextrin
Reported limits: No exact arm-specific n beyond ≥6; no curve-derived values added.
Sapacitabine 5 mg/kg + vorinostat
Model: Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size
Route: Sapacitabine oral; vorinostat intraperitoneal
Frequency: Each once daily
Treatment course: Sapacitabine: 4 days, 3-day break, another 4 days; vorinostat: 12 days starting the following day
Vehicle: Sapacitabine vehicle reported as 2.5% dimethylacetate and 9.75% emulphor; vorinostat in 40% hydroxypropyl-β-cyclodextrin.
Reported limits: No exact arm-specific n beyond ≥6; no curve-derived values added.
Sapacitabine 15 mg/kg + vorinostat
Model: Female nu/nu mice bearing subcutaneous MV4-11 xenografts; ≥6 mice per group; pair matched by tumour size
Route: Sapacitabine oral; vorinostat intraperitoneal
Frequency: Each once daily
Treatment course: Sapacitabine: 4 days, 3-day break, another 4 days; vorinostat: 12 days starting the following day
Vehicle: Sapacitabine vehicle reported as 2.5% dimethylacetate and 9.75% emulphor; vorinostat in 40% hydroxypropyl-β-cyclodextrin.
Reported limits: No exact arm-specific n beyond ≥6; no curve-derived values added.
Methods and source locations

Compound reported in the paper: Sapacitabine; Compound label in the paper: CYC682 / CS-682

Compound-level literature evidence; no certificate, catalog-number or lot equivalence established for A12801.

Methods: In vivo studies; Results: In vivo evaluation of sapacitabine and vorinostat in combination; Figure 5 and caption

Day-14 tumour growth: Exact values from Results; Figure 5 viewed for direction, arms and ±s.e.m. TGI is based on change from baseline, permitting values >100%. — Results: In vivo evaluation, day-14 paragraph; Figure 5

Between-group tumour response: Authors also report both combination treatments significant against appropriate controls by unpaired t-tests without exact pairwise values. — Results: In vivo evaluation, final paragraph

Vehicle control · Figure 5 and caption; In vivo studies methods; In vivo evaluation results

Sapacitabine 5 mg/kg · Figure 5 and caption; In vivo studies methods; In vivo evaluation results

Sapacitabine 15 mg/kg · Figure 5 and caption; In vivo studies methods; In vivo evaluation results

Vorinostat single agent · Figure 5 and caption; In vivo studies methods; In vivo evaluation results

Sapacitabine 5 mg/kg + vorinostat · Figure 5 and caption; In vivo studies methods; In vivo evaluation results

Sapacitabine 15 mg/kg + vorinostat · Figure 5 and caption; In vivo studies methods; In vivo evaluation results

Specifications

Manufacturer Adooq Bioscience
CAS Number 151823-14-2
Formula C26H42N4O5
Molecular Weight 490.63
Synonyms CYC 682; CS-682
SMILES
CCCCCCCCCCCCCCCC(=O)NC1=NC(=O)N(C=C1)[C@H]2[C@H]([C@@H]([C@H](O2)CO)O)C#N

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

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.

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] Serova M, Galmarini CM, Ghoul A, et al. Antiproliferative effects of sapacitabine (CYC682), a novel 2'-deoxycytidine-derivative, in human cancer cells. British journal of cancer (2007). PMID: 17637678 DOI: 10.1038/sj.bjc.6603896 Source material
  2. [2] George SL, Lorenzi F, King D, et al. Therapeutic vulnerabilities in the DNA damage response for the treatment of ATRX mutant neuroblastoma. EBioMedicine (2020). PMID: 32846370 DOI: 10.1016/j.ebiom.2020.102971 Source material
  3. [3] Green SR, Choudhary AK, Fleming IN. Combination of sapacitabine and HDAC inhibitors stimulates cell death in AML and other tumour types. British journal of cancer (2010). PMID: 20924380 DOI: 10.1038/sj.bjc.6605922 Source material

Publications

1 publication citing this product

  1. Sally L George, .et al. , EBioMedicine, 2020, Aug 23;59:102971 PMID: 32846370

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