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Fig. 1 · Structure
Cat. No.
A13203
CAS No.
1204144-28-4
Formula
C21H21N3O2S
Mol. Weight
379.48

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AZD1208

Cat. No. A13203 CAS 1204144-28-4

pan-Pim kinase inhibitor

AZD1208 is orally available, small molecule inhibitor of PIM kinases with potential antineoplastic activity.

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Publications for AZD1208

7 publications citing this product

  1. Corbin C Jensen, .et al. , J Cell Biol, 2023, Jun 5;222(6):e202208136 PMID: 37042842
  2. Jeremiah J Bearss, .et al. , EMBO Rep, 2021, Apr 7;22(4):e50835 PMID: 33586867
  3. Remy J, .et al. , Biochim Biophys Acta Mol Cell Res, 2019, Feb;1866(2):175-189 PMID: 30389373
  4. Andrea L. Casillas, .et al. , Clin Cancer Res, 2018, Jan 1; 24(1): 169-180 PMID: 29084916
  5. Jin H. Song, .et al. , Mol Cancer Ther, 2018, Dec;17(12):2710-2721 PMID: 30190422
  6. Sathish K.R. Padi, .et al. , Oncotarget, 2017, May 2; 8(18): 30199-30216 PMID: 28415816
  7. Lim R, .et al. , Mol Hum Reprod, 2017, Jun 1;23(6):428-440 PMID: 28333279
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Biological Activity

Bioactivity / Mechanism

AZD1208 is an ATP-competitive inhibitor of PIM1, PIM2 and PIM3. In the founding study, enzyme IC50 values at ATP Km were 0.4, 5.0 and 1.9 nM, respectively, increasing to 2.6, 164 and 17 nM at 5 mM ATP. These values describe the paper’s material, depicted with HCl, and are assay-dependent endpoints rather than treatment doses. [1]

In an independent recombinant assay using AZD1208 identified as AdooQ A13203-750, 100 nM AZD1208 suppressed PIM1-dependent phosphorylation of ABI2. This supports inhibition at a PIM1 substrate but does not establish a new IC50 or validate current product lots. [2]

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

Target & Activity

Target Activity Value
Pim1 (Cell-free assay) 0.4 nM
Pim3 (Cell-free assay) 1.9 nM
Pim2 (Cell-free assay) 5 nM

Cellular Effect

Cell Line Activity Value Description Reference
KMS-11 EC50 0.67 μM Antiproliferative activity against luciferase expressing human KMS11 cells after 72 hrs by Cell-TiterGlo assay [PMID: 26505898]
WI-38 IC50 > 10000 nM Growth inhibition of human WI38 cells after 48 hrs by CCK8 assay [PMID: 28523101]

In Vitro Studies

AZD1208 induced cell-cycle arrest and apoptotic/dead-cell staining in MOLM-16 AML cells after 72 hours. The phenotype was model-dependent: KG-1a and EOL-1 did not show the same arrest, and the authors reported no comparable marked apoptotic response in the other sensitive lines tested. The study’s material is depicted with HCl; equivalence to other forms was not established. [1]

ATP-dependent inhibition of purified PIM kinases

Biochemical assay · Purified human PIM1, PIM2 and PIM3 with BAD substrate [1]

AZD1208 inhibited all three PIM isoforms. Higher ATP reduced apparent potency, especially for PIM2; these enzyme endpoints are not cellular treatment concentrations.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
PIM1 / PIM2 / PIM3 enzyme activity at ATP KmIC50 0.4 / 5.0 / 1.9 nM[1]
PIM1 / PIM2 / PIM3 enzyme activity at 5 mM ATPIC50 2.6 / 164 / 17 nM[1]
PIM1 / PIM2 / PIM3 inhibition constantsKi 0.10 / 1.92 / 0.40 nM[1]

Literature-Reported Treatment Conditions

Treatment concentration
Concentration-response assays; ATP at Km or 5 mM.
Method
Purified-enzyme activity assay; inhibition constants fitted across ATP and compound concentrations.
Vehicle
DMSO stock; final assay vehicle fraction not specified in read main text.
Reported limits
Inhibitor concentration range, enzyme-assay incubation time and replicate counts not specified in read main text; SI not retrieved.
Methods and source locations

Compound reported in the paper: AZD1208; Compound label in the paper: AZD1208 (Figure 1 depicts HCl)

Results apply to the paper’s AZD1208 material, depicted with HCl; no quantitative equivalence to the catalog material or salt conversion is established.

Table 1; Results: AZD1208 is a potent and selective pan-Pim kinase inhibitor; Methods: Enzyme assays; Figure 1

PIM1 / PIM2 / PIM3 enzyme activity at ATP Km: Purified-enzyme assay with BAD substrate — Table 1, Enzyme IC50 at Km [ATP] row

PIM1 / PIM2 / PIM3 enzyme activity at 5 mM ATP: Purified-enzyme assay with BAD substrate — Table 1, Enzyme IC50 at 5 mM [ATP] row

PIM1 / PIM2 / PIM3 inhibition constants: Global fitting using Cheng-Prusoff or Morrison equation; 1 nM enzyme and 1.5 µM full-length BAD in Ki experiments. — Table 1 Ki row; Methods: Enzyme assays

Cell-cycle arrest and apoptosis in MOLM-16 cells

Cell-based study · MOLM-16 human AML cells; KG-1a and EOL-1 provide author-reported phenotype limits. [1]

At 72 hours, AZD1208 increased G0/G1 and subG1 populations and apoptotic/dead-cell staining in MOLM-16. KG-1a and EOL-1 did not show the same cell-cycle arrest, and no other sensitive line showed a comparable marked apoptotic response (reported in text, data not shown).

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell-cycle distribution and Annexin V/7-AAD populationsQualitative response Dose-dependent cell-cycle arrest and increase in apoptotic/dead cells; representative of 3 independent experiments.[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.1 and 1 µM; control labeled C in Figure 2.
Exposure duration
72 hours
Method
Propidium-iodide DNA-content cytometry and Annexin V/7-AAD cytometry.
Vehicle
DMSO stock; cytometry control labeled C without explicit vehicle fraction.
Reported limits
No exact numerical apoptosis percentages inferred from bars. Final vehicle fraction and initial well-specific density are not supplied for each plotted panel.
Methods and source locations

Compound reported in the paper: AZD1208; Compound label in the paper: AZD1208 (Figure 1 depicts HCl)

Results apply to the paper’s AZD1208 material, depicted with HCl; no quantitative equivalence to the catalog material or salt conversion is established.

Figure 2B–C and caption; Results: AZD1208 inhibits AML cell-line growth and can induce cell-cycle arrest and apoptosis; Methods: Cell cycle, cell size, and apoptosis

Cell-cycle distribution and Annexin V/7-AAD populations: DNA-content and apoptosis flow cytometry; negative phenotype observations in KG-1a and EOL-1 are text-only, data not shown. — Figure 2B–C, caption and adjacent Results

Inhibition of PIM1-dependent ABI2 phosphorylation

Biochemical assay · Recombinant GST-PIM1 with recombinant ABI2; MBP positive-control substrate; GST negative control described in methods. [2]

AZD1208 suppressed PIM1-dependent ABI2 phosphorylation in the recombinant assay. Figure S2a shows loss of the ABI2 autoradiographic signal with inhibitor, supporting a substrate-level PIM1 effect.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
ABI2 phosphorylation in the presence versus absence of AZD1208Qualitative autoradiography ABI2 phosphorylation was abrogated with AZD1208; no numerical inhibition percentage or IC50 reported for this assay.[2]

Literature-Reported Treatment Conditions

Treatment concentration
100 nM
Exposure duration
1 hour
Method
Radiolabeled ATP kinase reaction at 37°C, followed by SDS-PAGE, Coomassie staining and autoradiography.
Reported limits
Salt form, final vehicle fraction, ATP concentration and independent replicate count not specified in the read kinase-assay text.
Methods and source locations

Compound reported in the paper: AZD1208; Compound label in the paper: AZD1208 (AdooQ A13203-750)

Historical use of the named commercial material; no validation of current Adooq lots.

Figure S2a and caption; Results: Identification of ABI2 as a novel PIM substrate; Methods: Kinase assays and mass spectrometry; Reagents

ABI2 phosphorylation in the presence versus absence of AZD1208: Coomassie loading/protein visualization and autoradiography; MBP positive control in Figure S2a; GST negative control described in Methods. — Figure S2a, caption; adjacent Results; Methods: Kinase assays and mass spectrometry

In Vivo Studies

In a MOLM-16 xenograft model, oral AZD1208 given once daily for 14 days produced 89% tumor growth inhibition at 10 mg/kg and slight regression at 30 mg/kg versus vehicle. The higher dose was described as a typical maximum-tolerated dose on this schedule. These are preclinical results for the reported material, depicted with HCl, without salt-dose conversion. [1]

Oral AZD1208 in a MOLM-16 xenograft model

Animal study · MOLM-16 subcutaneous tumors in female CB17 SCID mice [1]

Repeated oral AZD1208 inhibited tumor growth versus vehicle over 14 days. The 30 mg/kg schedule was described as a typical maximum-tolerated dose; efficacy does not establish a broad safety margin.

Conditions shared by the study groups

Route
Oral gavage
Frequency
Once daily
Treatment course
14 days
Vehicle
0.5% hydroxypropyl methylcellulose
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
AZD1208 monotherapy versus vehicle
10 or 30 mg/kg (reported doses; no salt conversion).		Vehicle-treated mice; randomized allocation when tumors reached approximately 150–200 mm³.10 mg/kg: 89% tumor growth inhibition; 30 mg/kg: slight tumor regression. Figure 4A caption reports P < .001 for day-25 tumor size comparisons with vehicle and average ± SEM.[1]
AZD1208 monotherapy versus vehicle
Model: MOLM-16 subcutaneous xenografts in female CB17 SCID mice, 5–6 weeks old.
Reported limits: Methods report 10–15 mice/group generally; exact n for each Figure 4A group is not separately stated. Blinding is not specified in the read methods.
Methods and source locations

Compound reported in the paper: AZD1208; Compound label in the paper: AZD1208 (Figure 1 depicts HCl)

Results apply to the paper’s AZD1208 material, depicted with HCl; no quantitative equivalence to the catalog material or salt conversion is established.

Figure 4A and caption; Methods: In vivo studies; Results: AZD1208 efficacy and PK-PD in AML xenografts

AZD1208 monotherapy versus vehicle · Figure 4A and caption; Results: AZD1208 efficacy and PK-PD in AML xenografts; Methods: In vivo studies

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1204144-28-4
Applications pan-Pim kinase inhibitor
Formula C21H21N3O2S
Molecular Weight 379.48
SMILES
C1C[C@H](CN(C1)C2=C(C=CC=C2/C=C\3/C(=O)NC(=O)S3)C4=CC=CC=C4)N

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 70 mg/mL (184.45 mM)
Water Insoluble
Ethanol Insoluble

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] Keeton EK, McEachern K, Dillman KS, et al. AZD1208, a potent and selective pan-Pim kinase inhibitor, demonstrates efficacy in preclinical models of acute myeloid leukemia Blood (2014). PMID: 24363397 DOI: 10.1182/blood-2013-04-495366 Source material
  2. [2] Jensen CC, Clements AN, Liou H, et al. PIM1 phosphorylates ABI2 to enhance actin dynamics and promote tumor invasion J Cell Biol (2023). PMID: 37042842 DOI: 10.1083/jcb.202208136 Source material

Publications

7 publications citing this product

  1. Corbin C Jensen, .et al. , J Cell Biol, 2023, Jun 5;222(6):e202208136 PMID: 37042842
  2. Jeremiah J Bearss, .et al. , EMBO Rep, 2021, Apr 7;22(4):e50835 PMID: 33586867
  3. Remy J, .et al. , Biochim Biophys Acta Mol Cell Res, 2019, Feb;1866(2):175-189 PMID: 30389373
  4. Andrea L. Casillas, .et al. , Clin Cancer Res, 2018, Jan 1; 24(1): 169-180 PMID: 29084916
  5. Jin H. Song, .et al. , Mol Cancer Ther, 2018, Dec;17(12):2710-2721 PMID: 30190422
  6. Sathish K.R. Padi, .et al. , Oncotarget, 2017, May 2; 8(18): 30199-30216 PMID: 28415816
  7. Lim R, .et al. , Mol Hum Reprod, 2017, Jun 1;23(6):428-440 PMID: 28333279

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