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Fig. 1 · Structure
Cat. No.
A11105
CAS No.
602306-29-6
Formula
C18H21N5O2S
Mol. Weight
371.5

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AZD5438

Cat. No. A11105 CAS 602306-29-6

CDK inhibitor

AZD5438 is a potent inhibitor of cyclin-dependent kinase (CDK) 1, 2 and 9 (IC50 values are 16, 6 and 20 nM respectively).

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Biological Activity

Target & Activity

Target Activity Value
cdk2-cyclin E IC50 6 nM
cdk2-cyclin A IC50 45 nM
cdk5-p25 IC50 14 nM
cdk1-cyclin B1 IC50 16 nM
cdk9-cyclin T IC50 20 nM
cdk6-cyclin D3 IC50 21 nM
cdk4-cyclin D1 IC50 449 nM
cdk7-cyclin H IC50 821 nM

8 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
HCT-116 IC50 0.47 μM Antiproliferative activity against human HCT116 cells incubated for 48 hrs by MTT assay [PMID: 31254921]
HeLa IC50 0.73 μM Antiproliferative activity against human HeLa cells incubated for 48 hrs by MTT assay [PMID: 31254921]
HeLa IC50 1.2 μM Cytotoxicity against human HeLa cells assessed as reduction in cell viability after 48 hrs by resazurin dye based fluorescence assay [PMID: 30647879]
LoVo IC50 0.63 μM Antiproliferative activity against human LoVo cells assessed as BrdU incorporation after 48 hrs [PMID: 18815031]
LoVo IC50 0.8 μM Antiproliferative activity against human LoVo cells assessed as inhibition of BrdU incorporation after 48 hrs [PMID: 18996007]
LoVo IC50 0.8 μM Antiproliferative activity against human LoVo cells assessed as inhibition of BrdU incorporation after 48 hrs [PMID: 18986805]
MCF7 IC50 10.67 μM Antiproliferative activity against human MCF7 cells incubated for 48 hrs by MTT assay [PMID: 31254921]
MDA-MB-231 IC50 7.2 μM Antiproliferative activity against human MDA-MB-231 cells incubated for 48 hrs by MTT assay [PMID: 31254921]
PC-3 IC50 0.36 μM Antiproliferative activity against human PC3 cells incubated for 48 hrs by MTT assay [PMID: 31254921]

9 records · Scroll to view more

In Vitro Studies

In HN12 cells exposed to serial drug dilutions for 72 h, the reported cell viability result for AZD5438 was 3.852 µM, with vehicle-treated controls. In NCCIT cells, AZD5438 was assessed using cell confluence, with a reported IC50 of 1.38 μM. [1,2]

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

Cell viability assessment in HN12 cells

Cell-based study · HN12; n = 3 biological replicates/dose [1]

HN12 cells were exposed to serial drug dilutions for 72 h, with vehicle-treated controls. The reported cell viability result was 3.852 µM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
cell viabilityIC₅₀ 3.852 µM[1]

Literature-Reported Treatment Conditions

Exposure duration
72 h
Method
exposed in triplicate to a serial dilution of the drug
Reported limits
Not stated in the sentences used: dose, vehicle.
Methods and source locations

Compound reported in the paper: AZD5438

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Methods > Drug IC50 determination and drug synergism (S24, S25, S26); Results > The combination of AZD5438 and PD0325901 exhibits superior efficacy in suppressing HNSCC with high mutational burden compared to either treatment alone (S136, S147, S148)

cell viability: cell viability; comparator: vehicle-treated controls — Methods > Drug IC50 determination and drug synergism (S25); Results > The combination of AZD5438 and PD0325901 exhibits superior efficacy in suppressing HNSCC with high mutational burden compared to either treatment alone (S136)

Cell confluence assessment in NCCIT cells

Cell-based study · NCCIT cells [2]

NCCIT cells were treated with AZD5438 and assessed for cell confluence. The reported IC50 was 1.38 μM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
cell confluenceIC50 IC50 of 1.38 μM[2]

Literature-Reported Treatment Conditions

Reported limits
Not stated in the sentences used: dose, route, schedule, vehicle, control.
Methods and source locations

Compound reported in the paper: AZD5438

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Material and methods > Assessment of cell viability (S85); Results > No interference of AZD5438 with cisplatin anti-cancer activity in vitro and in mice (S137, S138)

cell confluence: cell confluence — Material and methods > Assessment of cell viability (S85); Results > No interference of AZD5438 with cisplatin anti-cancer activity in vitro and in mice (S138)

In Vivo Studies

In NCCIT tumor-bearing SCID mice, tumor volume increased at similar rates with vehicle alone and AZD5438 administered at 9.4 mg/kg by oral gavage. In FVB/NJ strain mice, AZD5438 at 35 mg/kg by oral gavage with cisplatin produced a 2.1-fold decrease in BUN values to 51±7 mg/dl compared with cisplatin alone. [2,3]

Tumor volume growth in NCCIT tumor-bearing mice

Animal study · NCCIT tumor-bearing SCID mice [2]

NCCIT tumor-bearing SCID mice received AZD5438 by oral gavage at 9.4 mg/kg. Normalized tumor volume increased at similar rates in the vehicle-only and AZD5438 groups.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
normalized tumor volume (to the initial volume at the onset of the treatment)Reported result the tumor volume increased at similar rates in the vehicle only and the AZD5438 group[2]

Conditions shared by the study groups

Route
oral gavage
Treatment course
twice daily via oral gavage at 9.4 mg/kg on days 1, 2, and 3 of each 7-day treatment cycle
Vehicle
10 % DMSO (#D2650, MilliporeSigma), 5 % Tween-80 (#HY-Y1891, MCE), 40 % PEG-300 (#HY-Y0873, MCE), and 45 % saline solution
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
AZD5438 9.4 mg/kgsaline/vehicle (Vehicle group)the tumor volume increased at similar rates in the vehicle only and the AZD5438 group[2]
AZD5438 9.4 mg/kg
Model: NCCIT tumor-bearing SCID mice
Methods and source locations

Compound reported in the paper: AZD5438

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Material and methods > Animal experiments > Multi-cycle cisplatin ototoxicity mouse model (S14); Material and methods > Animal experiments > Mouse xenograft model (S20, S26, S27, S29); Results > No interference of AZD5438 with cisplatin anti-cancer activity in vitro and in mice (S152); Fig. 3 legend (S177)

normalized tumor volume (to the initial volume at the onset of the treatment): normalized tumor volume (to the initial volume at the onset of the treatment); comparator: saline/vehicle (Vehicle group) — Results > No interference of AZD5438 with cisplatin anti-cancer activity in vitro and in mice (S152); Fig. 3 legend (S177)

AZD5438 9.4 mg/kg · Material and methods > Animal experiments > Mouse xenograft model (S26); Results > No interference of AZD5438 with cisplatin anti-cancer activity in vitro and in mice (S152)

colorimetric detection of BUN in FVB/NJ strain mice

Animal study · FVB/NJ strain mice [3]

Model: FVB/NJ strain mice. Treatment: 35 mg/kg. Result: 2.1-fold decrease in BUN values to 51±7 mg/dl.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
colorimetric detection of BUNBUN 51±7 mg/dl[3]

Conditions shared by the study groups

Route
oral gavage
Treatment course
45 minutes before injecting with cisplatin; twice daily for three consecutive days
Vehicle
10% DMSO (BP231-100, Fisher), 5% Tween 80 (P1754, Sigma-Aldrich), 40% PEG-E-300 (91462, Sigma-Aldrich), and 45% saline (0.9% NaCl)
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
AZD5438 35 mg/kgcisplatin alone treated mice2.1-fold decrease in BUN values to 51±7 mg/dl[3]
AZD5438 35 mg/kg
Model: FVB/NJ strain mice
Methods and source locations

Compound reported in the paper: AZD5438

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Methods > Administration of Drugs by Oral Gavage (S27, S28); Results > Oral Administration of AZD5438 or Dabrafenib Protected from Acute Cisplatin-Induced Renal Injury in Mice, Measured by Reduction in the Levels of Injury and Histopathology Biomarkers on Day 3 (S85, S89, S91, S93, S95)

colorimetric detection of BUN: colorimetric detection of BUN; comparator: cisplatin alone treated mice — Results > Oral Administration of AZD5438 or Dabrafenib Protected from Acute Cisplatin-Induced Renal Injury in Mice, Measured by Reduction in the Levels of Injury and Histopathology Biomarkers on Day 3 (S91, S93)

AZD5438 35 mg/kg · Methods > Administration of Drugs by Oral Gavage (S27, S28); Results > Oral Administration of AZD5438 or Dabrafenib Protected from Acute Cisplatin-Induced Renal Injury in Mice, Measured by Reduction in the Levels of Injury and Histopathology Biomarkers on Day 3 (S89, S93)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 602306-29-6
Applications CDK inhibitor
Formula C18H21N5O2S
Molecular Weight 371.5
SMILES
CC1=NC=C(N1C(C)C)C2=NC(=NC=C2)NC3=CC=C(C=C3)S(=O)(=O)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 68 mg/mL (183.06 mM)
Water Insoluble
Ethanol 68 mg/mL (183.06 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.

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] Chen F, Yang F, Popoola DO, et al. Dual CDK and MEK Inhibition potentiates CD8+ T cell-mediated antitumor immunity by inducing pyroptotic cell death in high-mutational head and neck cancer. J Exp Clin Cancer Res (2025). PMID: 41194215 DOI: 10.1186/s13046-025-03557-7 Source material
  2. [2] Huang Y, Zhang X, Vesanes E, et al. Oral AZD5438 is a clinically translatable otoprotectant against cisplatin-induced hearing loss. Neoplasia (2026). PMID: 41187663 DOI: 10.1016/j.neo.2025.101250 Source material
  3. [3] Pushpan CK, Kresock DF, Ingersoll MA, et al. Repurposing AZD5438 and Dabrafenib for Cisplatin-Induced AKI. J Am Soc Nephrol (2024). PMID: 37962623 DOI: 10.1681/ASN.0000000000000261 Source material

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