Fig. 1 · Structure

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Seliciclib (Roscovitine)

CDK Inhibitor

Roscovitine (Seliciclib) is a CDK inhibitor that preferentially inhibit multiple enzyme targets including CDK2, CDK7 and CDK9.

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Publications for Seliciclib

3 publications citing this product

  1. Abdel-Aziz S Shatat, .et al. , Purinergic Signal, 2024, May 27 PMID: 38801618
  2. Reiko Watanabe, .et al. , J Med Chem, 2021, Mar 11;64(5):2725-2738 PMID: 33619967
  3. Vimal Pandey, .et al. , Scientific Reports, 2019, 9, Article number: 5012 PMID: 30899038

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Biological Activity

Bioactivity / Mechanism

In mouse embryonic fibroblasts, R-roscovitine induced S-phase accumulation in wild-type cells, whereas CDK2-null cells lacked this response. This supports a role for CDK2 in the cell-cycle phenotype under these conditions. [1]

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

Target & Activity

Target Activity Value
CDK5/p35 IC50 0.16μM
Cdc2/CyclinB IC50 0.65μM
CDK2/CyclinA IC50 0.7μM
CDK2/CyclinE IC50 0.7μM
ERK2 IC50 14μM
GST-ERK1 IC50 30μM
ERK1 IC50 34μM
CDK4/CyclinD1 IC50 >100μM
CDK6/CyclinD3 IC50 >100μM
PKCα IC50 >100μM
PKCβ1 IC50 >100μM
PKCβ2 IC50 >100μM
PKCγ IC50 100μM
PKCε IC50 >100μM
PKCη IC50 >100μM
c-Src IC50 250μM
PKCδ IC50 >1000μM
PKCζ IC50 >1000μM
v-Abl IC50 >1000μM

19 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
786-0 GI50 25.1 μM Antiproliferative activity against human 786-0 cells after 72 hrs by ViaLight assay [PMID: 19128055]
A2780 GI50 12.5 μM Growth inhibition of cisplatin-resistant human A2780 cells after 96 hrs by sulforhodamine B assay [PMID: 21982796]
A2780 GI50 4.45 μM Growth inhibition of cisplatin-susceptible human A2780 cells after 96 hrs by sulforhodamine B assay [PMID: 21982796]
A-375 IC50 11.79 μM Antiproliferative activity against human A-375 cells assessed as reduction in cell growth incubated for 72 hrs by CCK-8 assay [PMID: 32361064]
A498 GI50 50.1 μM Antiproliferative activity against human A498 cells after 72 hrs by ViaLight assay [PMID: 19128055]
A549 IC50 > 10 μM Antiproliferative activity against human A549 cells measured after 72 hrs by CCK8 assay [PMID: 31272794]
A549 GI50 12.6 μM Antiproliferative activity against human A549 cells after 72 hrs by ViaLight assay [PMID: 19128055]
A549 IC50 14.14 μM Cytotoxicity against human A549 cells after 48 hrs by SRB assay [PMID: 23036956]
A549 IC50 14.7 μM Antiproliferative activity against human A549 cells after 3 days by SRB assay [PMID: 20361800]
A549 GI50 15 μM Antiproliferative activity against human A549 cells after 72 hrs by sulforhodamine B assay [PMID: 21080703]
A549 IC50 2.18 μM Cytotoxicity against human A549 cells after 48 hrs by MTT assay [PMID: 23623491]
ACHN GI50 12.6 μM Antiproliferative activity against human ACHN cells after 72 hrs by ViaLight assay [PMID: 19128055]
ACHN IC50 2.88 μM Cytotoxicity against human ACHN cells after 48 hrs by MTT assay [PMID: 23623491]
ASPC1 IC50 17767 nM Antiproliferative activity against human AsPC1 cells after 72 hrs by prestoblue assay [PMID: 30343954]
BXPC-3 IC50 15284 nM Antiproliferative activity against human BxPC3 cells after 72 hrs by prestoblue assay [PMID: 30343954]
Caco-2 IC50 10 μM Antiproliferative activity against human Caco2 cells after 48 hrs by Hoechst 33342 staining-based assay [PMID: 30655216]
Caco-2 IC50 10 μM Cytotoxicity against human Caco2 cells after 48 hrs by Hoechst-33342 staining-based imaging analysis [PMID: 21944287]
Caco-2 IC50 12.9 μM Cytotoxicity against human Caco2 cells assessed as cell viability after 48 hrs by Hoechst 33342 staining based assay [PMID: 28214231]
Caco-2 IC50 14 μM Cytotoxicity against human Caco-2 cells assessed as reduction in cell viability after 48 hrs [PMID: 34601029]
Caco-2 IC50 17 μM Cytotoxicity against human CaCo-2 cells assessed as reduction in cell viability incubated for 48 hrs by Hoechst-33342 staining based cell counting method (Rvb > 25 microM) [PMID: 33422908]

20 records · Scroll to view more

In Vitro Studies

R-roscovitine reduced WST-1 signal in AtT20 mouse corticotroph tumor cells at 10–20 μM over 24–48 h. Reduced Rb Thr821 phosphorylation and altered cell-cycle regulator expression accompanied the response. These cellular endpoints do not establish a purified-enzyme potency or an exclusively CDK2-mediated effect. [2]

CDK2 dependence of the cell-cycle response in mouse fibroblasts

Cell-based study · Immortalized wild-type and CDK2-null mouse embryonic fibroblasts [1]

R-roscovitine produced S-phase accumulation in wild-type MEFs; this response was absent in CDK2-null MEFs. The experiment supports CDK2 dependence of this cell-cycle phenotype.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
S-phase accumulation after R-roscovitine exposureQualitative cell-cycle distribution S-phase accumulation in wild-type MEFs; prevented by CDK2 loss; representative of two experiments[1]

Literature-Reported Treatment Conditions

Treatment concentration
10, 25 and 50 μM; untreated comparator
Exposure duration
48 h
Method
Cell exposure followed by DNA-content flow cytometry
Vehicle
Untreated control shown; DMSO was used for compound stocks. A separately labeled matched-vehicle FACS arm is not specified in the retrieved protocol/caption.
Reported limits
No numerical phase percentages are extracted from the bars. Figure 11B is representative of two experiments; no inferential statistics for phase distributions are given in its caption.
Methods and source locations

Compound reported in the paper: R-roscovitine (seliciclib; CYC202); Compound label in the paper: R-roscovitine

Results apply to the reported R-roscovitine material and model; no supplier-lot or formulation equivalence is established.

Figure 11B and caption (p. 31218); Cell Cycle Analysis (p. 31211); CDK2-null MEF Results (pp. 31214–31215); Figure 10B (p. 31217)

S-phase accumulation after R-roscovitine exposure: DNA-content FACScan analysis following methanol fixation, RNase and propidium iodide staining — Figure 11B and caption (p. 31218); Cell Cycle Analysis (p. 31211); CDK2-null MEF Results (pp. 31214–31215); Figure 10B (p. 31217)

Corticotroph cell response to R-roscovitine

Cell-based study · Mouse ACTH-secreting AtT20 corticotroph tumor cells [2]

R-roscovitine lowered WST-1 signal after 24 and 48 h. Immunoblots showed reduced Rb Thr821 phosphorylation with changes in cell-cycle regulators.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
WST-1 proliferation-assay signalRelative WST-1 signal Decreased at 10 and 20 μM at 24 and 48 h; mean ± SE; **P < 0.01 as captioned; no exact bar values extracted[2]
Rb Thr821 phosphorylation and cell-cycle regulatory proteinsQualitative immunoblot response Reduced phospho-Rb Thr821 and cyclin E; increased p27, p57 and p21[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 and 20 μM
Exposure duration
24 and 48 h for WST-1; immunoblot exposure duration not established in retrieved main text
Method
Cell treatment; WST-1 assay and immunoblotting
Vehicle
0.2% DMSO
Reported limits
Sample size and detailed assay implementation are not specified in the retrieved main Figure 4 caption; SI Methods were not retrieved. WST-1 is a metabolic assay and does not alone distinguish growth arrest from cell death.
Methods and source locations

Compound reported in the paper: R-roscovitine (seliciclib; CYC202); Compound label in the paper: R-roscovitine

Results apply to the reported R-roscovitine material and model; no supplier-lot or formulation equivalence is established.

Figure 4A–B and caption; Results: R-Roscovitine Action in Mouse Corticotroph Tumor Cells

WST-1 proliferation-assay signal: WST-1 assay — Figure 4A–B and caption; Results: R-Roscovitine Action in Mouse Corticotroph Tumor Cells

Rb Thr821 phosphorylation and cell-cycle regulatory proteins: Immunoblot; total Rb and β-actin displayed in Figure 4B — Figure 4A–B and caption; Results: R-Roscovitine Action in Mouse Corticotroph Tumor Cells

In Vivo Studies

In mice bearing AtT20 corticotroph tumors, R-roscovitine at 150 mg/kg by oral gavage twice daily, 5 days per week for 3 weeks, lowered serum corticosterone relative to vehicle. This finding is specific to the reported endocrine tumor model. [2]

Corticosterone response in mice bearing corticotroph tumors

Animal study · Athymic nude mice approximately 6–8 weeks old bearing subcutaneous AtT20 corticotroph tumor xenografts [2]

Oral R-roscovitine reduced serum corticosterone relative to vehicle in this corticotroph tumor model.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Serum corticosterone after treatmentConcentration (mean ± SE) Vehicle: 1,046 ± 109 ng/mL; R-roscovitine: 561 ± 72 ng/mL; n = 13–14 mice per group; P < 0.005 (Results)[2]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Twice daily, 5 days per week
Treatment course
3 weeks; treatment started 3 days after tumor-cell inoculation
Vehicle
Vehicle comparator; composition not established from retrieved main text
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
R-roscovitine versus vehicle
150 mg/kg
Mice randomized to R-roscovitine or vehicle; reported n = 13–14 per groupSerum corticosterone was lower with R-roscovitine: 561 ± 72 versus 1,046 ± 109 ng/mL, mean ± SE; P < 0.005 (Results).[2]
R-roscovitine versus vehicle
Model: Athymic nude mice approximately 6–8 weeks old bearing subcutaneous AtT20 corticotroph tumor xenografts
Reported limits: Sex, exact group-specific n within the reported 13–14 range, vehicle composition, blinding and hormone-assay implementation were not established from the retrieved main text; SI was not retrieved. This is an endocrine tumor model, not a general efficacy or safety result.
Methods and source locations

Compound reported in the paper: R-roscovitine (seliciclib; CYC202); Compound label in the paper: R-roscovitine

Results apply to the reported R-roscovitine material and model; no supplier-lot or formulation equivalence is established.

Figure 5D and caption; Results: R-Roscovitine Inhibits in Vivo Corticotroph Tumor Growth and ACTH Expression

Serum corticosterone after treatment: Serum corticosterone measurement; detailed assay procedure is in unretrieved SI rather than the retrieved main text — Figure 5D and caption; Results: R-Roscovitine Inhibits in Vivo Corticotroph Tumor Growth and ACTH Expression

R-roscovitine versus vehicle · Figure 5D and caption; Results: R-Roscovitine Inhibits in Vivo Corticotroph Tumor Growth and ACTH Expression

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 186692-46-6
Applications CDK Inhibitor
Formula C19H26N6O
Molecular Weight 354.5
Synonyms CYC202; Roscovitine
SMILES
CC[C@H](CO)NC1=NC2=C(C(=N1)NCC3=CC=CC=C3)N=CN2C(C)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 69 mg/mL (194.67 mM)
Water Insoluble
Ethanol 6 mg/mL (16.92 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
4 mg/mL
Vehicle
1% DMSO+10% Tween 80+20% N-N-dimethylacetamide+69% PEG 400

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] Bach S, Knockaert M, Reinhardt J, et al. Roscovitine targets, protein kinases and pyridoxal kinase. Journal of Biological Chemistry (2005). PMID: 15975926 DOI: 10.1074/jbc.m500806200 Source material
  2. [2] Liu NA, Jiang H, Ben-Shlomo A, et al. Targeting zebrafish and murine pituitary corticotroph tumors with a cyclin-dependent kinase (CDK) inhibitor. Proceedings of the National Academy of Sciences of the United States of America (2011). PMID: 21536883 DOI: 10.1073/pnas.1018091108 Source material

Publications

3 publications citing this product

  1. Abdel-Aziz S Shatat, .et al. , Purinergic Signal, 2024, May 27 PMID: 38801618
  2. Reiko Watanabe, .et al. , J Med Chem, 2021, Mar 11;64(5):2725-2738 PMID: 33619967
  3. Vimal Pandey, .et al. , Scientific Reports, 2019, 9, Article number: 5012 PMID: 30899038

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