Palbociclib (PD0332991) Isethionate

Licensed and Manufactured by Pfizer Catalog No.S1579

Palbociclib (PD0332991) Isethionate Chemical Structure

Molecular Weight(MW): 573.66

Palbociclib (PD0332991) Isethionate is a highly selective inhibitor of CDK4/6 with IC50 of 11 nM/16 nM in cell-free assays. It shows no activity against CDK1/2/5, EGFR, FGFR, PDGFR, InsR, etc. Phase 3.

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  • (C) In vivo treatment of Tg:Pomc-Pttg;Pomc-eGFP embryos with small-molecule CDK inhibitors (50μM) or 0.2% DMSO as control from 18 to 40 hpf. One hundred to one hundred fifty embryos were treated with each compound. Representative images of live embryos are shown with gross morphology (Right) and pituitary Pomc-GFP–positive cells at higher magnification (Left) at 40 hpf. Embryos exposed to flavopiridol developed early developmental defect before pituitary POMC cell ontogeny occurs. (D) Relative expression of pituitary Pomc-eGFP fluorescence analyzed using Volocity 5.2 software (Improvision; mean ±SE of relative expression, n = 7). (E) R-roscovitine specifically suppresses expansion of pituitary POMC cells overexpressing zPttg from 18 to 48 hpf. Double transgenic Tg:Pomc-Pttg;Prl-RFP embryos were generated by breeding Tg:Pomc-Pttg fish with a previously generated PRL-RFP transgenic line, in which RFP was targeted to pituitary lactotrophs by a zebrafish Prolactin promoter (34). Representative fluorescent microscopy of pituitary POMC-eGFP (a and b) and PRL-RFP (c and d) expression in live Tg:Pomc-Pttg; Pomc-eGFP and Tg:Pomc-Pttg;Prl-RFP embryos treated with 0.2% DMSO (a and c) or 50 μM R-roscovitine (b and d). (F) Relative expression of pituitary POMC-eGFP or PRL-RFP fluorescence were analyzed (mean ±SE of relative expression; n = 10). Results represent one of three similar experiments;*P < 0.02 and **P < 0.000005. (Scale bar, 50 μm.)

    PNAS 2011 108(20), 8414-9. Palbociclib (PD0332991) Isethionate purchased from Selleck.

    Immunoblot analysis of PD0332991-induced senescence in MEL10 cells. Cells were treated with indicated concentrations of PD0332991 with or without 10 nM rapamycin. After 1 day, cells were lysed and immunoblotting was performed with the indicated antibodies.

    Cell Cycle 2013 12(18), 3063-9. Palbociclib (PD0332991) Isethionate purchased from Selleck.

  • HT29 cells were treated with DMSO control, 1 uM selumetinib (Sel) or 5 uM PD0332991 (991) for 24 or 48 h after which time cells were lysed, subjected to SDS/PAGE and immunoblotted with the indicated antibodies.

    Biochem J 2014 459(3), 513-24. Palbociclib (PD0332991) Isethionate purchased from Selleck.

    Potentiation of SFN-induced cytotoxicity by a panel of CDK inhibitors in MDA-MB-231 cells. The fraction of cells killed (Fa ±SEM) by SFN in the presence of DMSO (vehicle) or a fixed concentration (0.2 uM) of PD0332991. The fraction of cells killed by CDK inhibitors at a fixed concentration of 0.2 uM is shown for comparison [dashed lines; gray shading (±SEM)]. MDE-CI analysis of drug interactions in the upper panels. CIs as a function of SFN concentration are shown. Black, gray, and white bars denote synergistic (CI < 0.9), additive (CI = 0.9-1.1), or antagonistic interactions (CI > 1.1), respectively. Synergistic ratios and SFN-EC50 are indicated. Data are representative of two to three independent experiments.

    Neoplasia 2013 15(8), 939-51. Palbociclib (PD0332991) Isethionate purchased from Selleck.

  •  

    Patient tumor cell sensitivity to combinatorial treatment with histone deacetylase (HDAC)/cyclin-dependent kinase (CDK) inhibitors in 3-D culture. The effect of each drug or drug combination was assessed by fluorescent dye to identify live (green) and dead cells (red). Cells from breast reduction patients were used as non-cancer control in the assay.

    Pharmacogenomics J 2013 13(1), 94-104. Palbociclib (PD0332991) Isethionate purchased from Selleck.

    Western blot analysis shows inhibition of Rb phosphorylation at the protein level, with inhibition of PD-0332991 observed at 2uM in the PDGF-B; Ink4a-ARF deficient line after only 24 hours of treatment.

    PLoS One 2013 8(10), e77639. Palbociclib (PD0332991) Isethionate purchased from Selleck.

  •  

    Cdk4 is upregulated in ARMS and mMSCs transfected with PAX7-FKHR fusion gene (MP7F), and can be specifi cally inhibited. D: IF results showing overexpression of cdk4 in MP7F cells compared to parental mMSCs and reduced expression of cdk4 after treatment of MP7F cells with the cdk4 inhibitor, PD-0332991. E: IF results showing MyoD1 expression in parental mMSCs cells, and MP7F cells untreated and after treatment with the cdk4 inhibitor, PD-0332991.

    Clin Transl Oncol 2012 14(3), 197-206 . Palbociclib (PD0332991) Isethionate purchased from Selleck.

    Different breast cancer cell lines were seeded in 96 well plates and treated with different concentrations of PD0332991. After 72h, cell viability was assessed by MTT. Data shows that these cancer cell lines had a better response to CDK4/6 inhibition than the less tumorigenic MCF10A-Ras cells.

    Helen Sadik from Johhns Hopkins University. Palbociclib (PD0332991) Isethionate purchased from Selleck.

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Biological Activity

Description Palbociclib (PD0332991) Isethionate is a highly selective inhibitor of CDK4/6 with IC50 of 11 nM/16 nM in cell-free assays. It shows no activity against CDK1/2/5, EGFR, FGFR, PDGFR, InsR, etc. Phase 3.
Features The 1st specific inhibitor for CDK4/6 to show promise in multiple cancers.
Targets
CDK4/CyclinD3 [1]
(Cell-free assay)
CDK4/CyclinD1 [1]
(Cell-free assay)
CDK6/CyclinD2 [1]
(Cell-free assay)
9 nM 11 nM 15 nM
In vitro

PD 0332991 exhibits absolute selectivity for CDK4/6 with little or no activity against other CDKs. PD 0332991 is effective at reducing Rb phosphorylation at Ser780 and Ser795 in MDA-MB-435 breast carcinoma cells with IC50 of 66 nM and 63 nM, respectively. PD 0332991 is a potent inhibitor of cell growth and suppresses DNA replication by preventing cells from entering S phase. PD 0332991 inhibits thymidine incorporation into the DNA of Rb-positive human breast (such as MDA-MB-435, MCF-7), colon (H1299), and lung carcinomas (Colo-205) as well as human leukemias (CRRF-CEM and K562), with IC50 values ranging from 0.04-0.17 μM. PD 0332991 significant increases the percentage of MDA-MB-453 in G1 period. [1] PD 0332991 inhibits phosphorylation of Rb in cycling CD138+ primary bone marrow myeloma cells, nontransformed primary B cells, MM1.S and CAG HMCLs cells line with IC50 of <0.1 μM, 0.05 μM, and 60-70 nM, respectively. PD 0332991 treatment also induces G1 arrest of CD138+ primary bone marrow myeloma and nontransformed primary B cells. PD 0332991 induces G1 arrest in MM1.S with IC50 of ~0.05 μM. [2] PD 0332991 preferentially inhibits proliferation of luminal estrogen receptor-positive (including HER2-positive) human breast cancer cell lines. PD 0332991 increases gene expression of pRb and cyclin D1 and decreases gene expression of CDKN2A (p16) in most sensitive lines. PD 0332991 enhances sensitivity to tamoxifen in cell lines with conditioned resistance to ER blockade. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
H157 NH7PNJdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MljONE0yODBizszN M2jSblczKGh? MV\JR|UxRTlizszN Moj0NlY{QTB|NEK=
H2170 MmLJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3LHcVAuOTByIN88US=> NY\kRYtOPzJiaB?= MVPJR|UxRTVizszN M37pZ|I3OzlyM{Sy
H520 M3PUUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jGRVAuOTByIN88US=> NUDJNVVCPzJiaB?= MmfuTWM2OD1yLkezJO69VQ>? M1XrR|I3OzlyM{Sy
H596 M37vRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{fwWFAuOTByIN88US=> NWX4RWZNPzJiaB?= MnrmTWM2OD1zMjFOwG0> NVnwfmJTOjZ|OUCzOFI>
IMR-32 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH;ONos1QMLiaB?= M{jGdmROW09? NV7HOHdVUUN3ME2yOlEhdk1? NEfrVmMzPjJ{NUGyNy=>
SH-SY5Y M3iwS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1XJ[lQ5yqCq MlrMSG1UVw>? NV;FcpRDUUN3ME22O|Yhdk1? M1vDZ|I3OjJ3MUKz
NGP MmfSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV[zdnBjPDkEoHi= NHvNVGtFVVOR MkLXTWM2OD1{LkC3O{DPxE1? M1;lelI3OjJ3MUKz
SH-EP MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHvWWXM1QMLiaB?= M4O5b2ROW09? NVnmWXVrUUN3ME2yMlIyOSEQvF2= NWfvW4d7OjZ{MkWxNlM>
IMR-32 NUfmOmQ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MW[xJO69VQ>? NETSO|AzPCCq NHrET3pFVVOR NXrvSVJocW6mdXPld{BIOSCjcoLld5Q> NImxNFAzPjJ{NUGyNy=>
SH-SY5Y Mo\rS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4ni[FEh|ryP NFS1d|MzPCCq M1TOPWROW09? M4\mUYlv\HWlZYOgS|Eh[XK{ZYP0 NILmW|IzPjJ{NUGyNy=>
NGP MmT0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3;vZlEh|ryP NXvseJNTOjRiaB?= M2nERWROW09? NG\GRnJqdmS3Y3XzJGcyKGG{cnXzeC=> MYKyOlIzPTF{Mx?=
SH-EP NXzyOmU6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXuxJO69VQ>? MVeyOEBp NIjZZXNFVVOR Mni0bY5lfWOnczDHNUBienKnc4S= MWKyOlIzPTF{Mx?=
NGP M1vtemZ2[3Srb36gRZN{[Xl? MkXRNE0yKM7:TR?= M1rOOlI1KGh? MonMSG1UVw>? Mn7xdoVlfWOnczD0bIUh\XiycnXzd4lwdiCxZtMgWG9ROkFuwrDDR25GOixiYX7kxsBVUzIEoHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ MYCyOlIzPTF{Mx?=
IMR-32 MnrmSpVkfGmxbjDBd5NigQ>? NWLZeHFIOC1zIN88US=> MVKyOEBp MlPPSG1UVw>? NVr5d4h1emWmdXPld{B1cGViZYjwdoV{e2mxbjDv[uKhXE:SMlGsxsBES06HMjygZY5lyqCWS{JCpIlvKGFiZH;z[U1l\XCnbnTlcpQhdWGwbnXy M2fEdVI3OjJ3MUKz
U-CH2 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1qxRlAuOSEQvF2= Mm\WO|IhcA>? MXHJR|UxRTVyLkKgcm0> MXyyOlE5Ozl{NR?=
U-CH3 NInlW4VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYSwMVEh|ryP NIjkc3Q4OiCq MWDJR|UxRTV{IH7N M3TTSFI3OTh|OUK1
U-CH6 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlPONE0yKM7:TR?= NGnWd5E4OiCq MkXGTWM2OD17MDDuUS=> NIPpPWwzPjF6M{myOS=>
U-CH7 M{HGO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn7CNE0yKM7:TR?= NH3BdW44OiCq M13vd2lEPTB;OUigcm0> MmPHNlYyQDN7MkW=
U-CH11 NWnXW3d4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3vIW|AuOSEQvF2= MlfUO|IhcA>? M2XocmlEPTB;M{SwJI5O M1\CbFI3OTh|OUK1
MCF7 MXjGeYN1cW:wIFHzd4F6 NGXsZVAzNjVvMkWwJI5O M1HFNlI1KGh? NYfj[5g3emWmdXPld{BT[iCyaH;zdIhwenmuYYTpc44> NXzrWJByOjV7OUG4NVc>
MV4-11 NGHzUWZCeG:ydH;zbZMhSXO|YYm= M4XyZ|AvPSEQvF2= M{LPb|I1KGh? NGe5dGdmdmijbnPld{BieG:ydH;zbZMhcW6mdXPl[EBjgSC|b4Lh[oVvcWJiYX7kJGFEOjJy NV:4VXdiOjV2OEe5NVc>
MOLM13 MYfBdI9xfG:|aYOgRZN{[Xl? NWX5NVB5OC53IN88US=> MnTPNlQhcA>? M4LYboVvcGGwY3XzJIFxd3C2b4Ppd{BqdmS3Y3XkJIJ6KHOxcnHm[Y5q[iCjbnSgRWMzOjB? NYHMTpJXOjV2OEe5NVc>
MOLM13-ITD alone MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{ewS2lEPTB;MD6wPFkhyrFiMD6wNFkh|ryP MXGyOVQ5PzlzNx?=
MV4-11-ITD alone NVroRlZuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3kfYFEUUN3ME2wMlA6OiEEsTCwMlAxQCEQvF2= NEnhRWMzPTR6N{mxOy=>
MOLM13-ITD/D835Y Mn3mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkG4TWM2OD1yLkGxOEDDuSByLkCxNUDPxE1? NUjYNXVWOjV2OEe5NVc>
MV4-11-ITD/D835V MnjDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHG3[VVKSzVyPUCuNVE3KMLzIECuNFEyKM7:TR?= M4nG[|I2PDh5OUG3
MV4-11-ITD/D835V NG\WZ2RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGjifHVKSzVyPUCuNVAzKMLzIECuNFA3KM7:TR?= NXH6[I4zOjV2OEe5NVc>
MV4-11-ITD/F691L M4Lye2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3;QTGlEPTB;MD6xNVIhyrFiMD6wNVUh|ryP MUmyOVQ5PzlzNx?=
MV4-11-ITD/N841K M3nlRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2XmNGlEPTB;MD6xNVMhyrFiMD6wNFIh|ryP MWWyOVQ5PzlzNx?=
U937-FLT3 WT NWHo[4JDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVPJR|UxRTBwMUCyJOKyKDBwMEGzJO69VQ>? M3vvRVI2PDh5OUG3

... Click to View More Cell Line Experimental Data

In vivo PD 0332991(150 mg/kg) produces rapid Colo-205 colon carcinoma xenografts regressions and a corresponding tumor growth delay. PD 0332991 (150 mg/kg) induces complete tumor stasis and cell kill in MDA-MB-435 breast carcinoma. PD 0332991 (150 mg/kg) also induces significant tumor regression in mice bearing the SF-295 glioblastoma xenografts, and in ZR-75-1 breast and PC-3 prostate tumor models (complete suppression of tumor growth). PD 0332991 (150 mg/kg) suppresses Rb Ser780 phosphorylation in MDA-MB-435 breast carcinoma over the full 24-hour period. PD 0332991 (150 mg/kg) down-regulates expression of four E2F-regulated genes CDC2, CCNE2, TK1, and TOP2A in Colo-205 carcinoma xenografts. [1] PD 0332991 also rapidly inhibits myeloma tumor growth. [2]

Protocol

Kinase Assay:[4]
+ Expand

CDK activity assays:

CDK assays for IC50 determinations and kinetic evaluation are performed in 96-well filter plates. All CDK-cyclin kinase complexes are expressed in insect cells through baculovirus infection and purified. The substrate for the assays is a fragment (amino acids 792–928) of pRb fused to GST (GST•RB-Cterm). The total reaction volume is 0.1 mL containing a final concentration of 20 mM Tris-HCl, pH 7.4, 50 mM NaCl, 1 mM dithiothreitol, 10 mM MgCl2 25 μM ATP (for CDK4-cyclin D1, CDK6-cyclin D2, and CDK6-cyclin D3) containing 0.25 μCi of [γ-32P]ATP, 20 ng of enzyme, 1 μg of GST•RB-Cterm, and appropriate dilutions of inhibitor. All components except the [γ-32P]ATP are added to the wells, and placed on a plate mixer for 2 min. The reaction is started by adding the [γ-32P]ATP, and incubated at 25℃ for 15 min. The reaction is terminated by addition of 0.1 mL of 20% trichloroacetic acid, and the plate is kept at 4 ℃ for at least 1 hr to allow the substrate to precipitate. The wells are then washed five times with 0.2 mL of 10% trichloroacetic acid, and radioactive incorporation is determined with a β plate counter.
Cell Research:[3]
+ Expand
  • Cell lines: Human breast cancer cells MDA-MB-435
  • Concentrations: 2 μM
  • Incubation Time: 6 days
  • Method: Cells are seeded in duplicate at 5,000 to 10,000 cells per well in 24-well plates. The day after plating, different concentrations of PD 0332991 are added. Control wells without drug are also seeded. At the end of incubation, cells are trypsinizated and placed in Isotone solution and counted immediately using a Coulter Z2 particle counter.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Human colon carcinoma xenografts Colo-205
  • Formulation: Solution in sodium lactate buffer (50 mM, pH 4.0)
  • Dosages: 150 mg/kg
  • Administration: o.p. injection every day
    (Only for Reference)

Solubility (25°C)

In vitro Water 10 mg/mL warmed (17.43 mM)
DMSO Insoluble
Ethanol Insoluble
In vivo Add solvents individually and in order:
saline (with warming)
10mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 573.66
Formula

C24H29N7O2.C2H6O4S

CAS No. 827022-33-3
Storage powder
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03007979 Not yet recruiting Breast Cancer|Breast Carcinoma|Cancer of Breast|Malignant Tumor of Breast Washington University School of Medicine February 28, 2017 Phase 2
NCT02907918 Not yet recruiting Breast Cancer|Cancer of Breast|Breast Carcinoma Washington University School of Medicine|Pfizer February 28, 2017 Phase 2
NCT01209598 Completed Sarcoma|Liposarcoma Memorial Sloan Kettering Cancer Center|Pfizer September 23, 2010 Phase 2
NCT03054363 Not yet recruiting Breast Cancer University of Colorado, Denver March 2017 Phase 1|Phase 2
NCT03024489 Not yet recruiting Head and Neck Cancer|Locally Advanced|Unresectable Mahidol University February 2017 Phase 1|Phase 2
NCT02947685 Not yet recruiting HER-2 Positive Breast Cancer|Estrogen Receptor Positive Breast Cancer Alliance Foundation Trials, LLC.|Pfizer|German Breast Group (GBG)|Fondazione Michelangelo|PrECOG, LLC.|The Australia and New Zealand Breast Cancer Trials Group (ANZBCTG)|Alliance Foundation Trials Biorepository - Washington State University|Alliance Foundation Trials Central Imaging Core Lab - Ohio State University|Mastering Breast Cancer Initiative, LLC|Mayo Clinic Statistics and Data Center|INC Research|SOLTI Breast Cancer Research Group February 2017 Phase 3

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

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Frequently Asked Questions

  • Question 1:

    What is the best vehicle for palbociclib for in vitro and in vivo?

  • Answer:

    You can use water for vitro use and Saline for vivo use.

  • Question 2:

    Could you please tell me what is the difference between the two palbociclib products that you sell: S1579 and S1116 ?

  • Answer:

    This two compounds are different Palbociclib salt. S1579 is the Isethionate salt, and the S1116 is the HCl salt. you can use S1116 for oral administration while S1579 is more suitable for I.P. administration. http://mct.aacrjournals.org/content/3/11/1427.long

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID