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Fig. 1 · Structure
Cat. No.
A11047
CAS No.
802539-81-7
Formula
C25H32N8O
Mol. Weight
460.6

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Milciclib (PHA-848125)

Cat. No. A11047 CAS 802539-81-7

CDK Inhibitor

PHA-848125 (Milciclib) is an orally bioavailable inhibitor of CDKs and TRKA with potential antineoplastic activity.

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Biological Activity

Target & Activity

Target Activity Value
CDK2/CyclinA IC50 45nM
TrkA IC50 53nM
CDK7/CyclinH IC50 150nM
CDK4/CyclinD1 IC50 160nM
CDK5/p35 IC50 265nM
CDK2/CyclinE IC50 363nM
CDK1/CyclinB IC50 398nM

7 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
A2780 IC50 0.2 μM Antiproliferative activity against human A2780 cells after 72 hrs by cell Titer_Glo assay [PMID: 19603809]
HEK-293T IC50 1.5 μM Antiproliferative activity against HEK293T cells measured after 72 hrs by CellTiter-Blue assay [PMID: 28792760]
HeLa IC50 4 μM Cytotoxicity against human HeLa cells assessed as reduction in cell viability after 48 hrs by resazurin dye based fluorescence assay [PMID: 30647879]
MDA-MB-231 IC50 0.31 μM Antiproliferative activity against human MDA-MB-231 cells measured after 72 hrs by CellTiter-Blue assay [PMID: 28792760]
MM1.S IC50 0.72 μM Antiproliferative activity against human MM1S cells measured after 72 hrs by CellTiter-Blue assay [PMID: 28792760]
Sf9 IC50 0.22 μM Inhibition of GST-tagged CDK4/cyclin D1 (unknown origin) expressed in Baculovirus infected Sf9 cells using RPPTLSPIPHIPR peptide as substrate in presence of [gamma-33P]-ATP by radiometric filter binding assay [PMID: 30234987]
Sf9 IC50 0.27 μM Inhibition of GST-tagged CDK7/cyclinH/MAT1 (unknown origin) expressed in Baculovirus infected Sf9 cells using YSPTSPS-2 KK peptide as substrate as substrate in presence of [gamma-33P]-ATP by radiometric filter binding assay [PMID: 30234987]
Sf9 IC50 0.383 μM Inhibition of GST-tagged CDK5/p25 (unknown origin) expressed in Baculovirus infected Sf9 cells using histone H1 as substrate as substrate in presence of [gamma-33P]-ATP by radiometric filter binding assay [PMID: 30234987]
Sf9 IC50 0.59 μM Inhibition of His-tagged CDK2/cyclin E (unknown origin) expressed in Baculovirus infected Sf9 cells using histone H1 as substrate in presence of [gamma-33P]-ATP by radiometric filter binding assay [PMID: 30234987]
Sf9 IC50 1.2 μM Inhibition of His-tagged CDK1/cyclin B1 (unknown origin) expressed in Baculovirus infected Sf9 cells using histone H1 as substrate in presence of [gamma-33P]-ATP by radiometric filter binding assay [PMID: 30234987]
Sf9 IC50 7.7 μM Inhibition of GST-tagged CDK9/CyclinT1 (unknown origin) expressed in Baculovirus infected Sf9 cells using YSPTSPS-2 KK peptide as substrate as substrate in presence of [gamma-33P]-ATP by radiometric filter binding assay [PMID: 30234987]

11 records · Scroll to view more

In Vitro Studies

In a cell viability study using GTML2 cells, Milciclib targeted MB cells more effectively than normal NSCs, with respective IC50 values of 0.95 μM and 5.5 μM. In HCT116 cells, Milciclib induced concentration-dependent G1 phase arrest with corresponding decreases in the S and G2/M phases. The sub-G1 population remained low at 1.85% after 24 h of treatment with 800 nM Milciclib. [1,2]

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

Milciclib effects on cell viability

Cell-based study · GTML2 cells [1]

GTML2 cells were treated with Milciclib for 72 h to assess cell viability. The reported IC50 values were 0.95 μM for MB cells and 5.5 μM for normal NSCs, indicating greater effectiveness against MB cells.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell viabilityIC50 IC50 0.95 μM[1]

Literature-Reported Treatment Conditions

Treatment concentration
0–15 μM
Exposure duration
72 h
Reported limits
Not stated in the sentences used: route, vehicle, control.
Methods and source locations

Compound reported in the paper: Milciclib

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

Results > CDK and BET bromodomain inhibitors target MYC proteins (S9, S14, S20); Materials and methods > Viability assay (S138)

Cell viability: Cell viability — Results > CDK and BET bromodomain inhibitors target MYC proteins (S14); Materials and methods > Viability assay (S138)

Milciclib induces cell cycle arrest

Cell-based study · HCT116 [2]

HCT116 cells were treated with Milciclib for 24 h, and cell cycle distribution was assessed by flow cytometry. Milciclib induced concentration-dependent G1 arrest with corresponding decreases in S and G2/M phases; the sub-G1 fraction remained low at 1.85% after treatment with 800 nM.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
flow cytometry to analyze cell cycle distributioncell cycle distribution 1.85%[2]

Literature-Reported Treatment Conditions

Treatment concentration
200, 400, and 800 nM
Exposure duration
24 h of treatment
Method
added to the culture medium
Vehicle
dimethyl sulfoxide (DMSO)
Methods and source locations

Compound reported in the paper: Milciclib

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

Materials and methods > Cell culture and drugs (S5); Materials and methods > Cell cycle assay (S30); Results > The CDK2 inhibitor Milciclib induces cell cycle arrest by inhibiting activated CDK2 in colorectal cancer (S73, S74, S75, S76, S77); FIGURE 2 legend (S128)

flow cytometry to analyze cell cycle distribution: flow cytometry to analyze cell cycle distribution; comparator: control group — Results > The CDK2 inhibitor Milciclib induces cell cycle arrest by inhibiting activated CDK2 in colorectal cancer (S74, S75, S76, S77)

In Vivo Studies

Milciclib was administered orally to NOD scid gamma mice bearing subcutaneous H460 xenografts, with vehicle as the comparator; mice were fasted overnight. PET imaging showed that Milciclib blocked xenograft glucose consumption by 30.4 ± 2.5% at 24 h after the first treatment. [3]

Milciclib Effects on Xenograft Glucose Consumption

Animal study · H460 xenografts were implanted into the subcutaneous space of NOD scid gamma mice [3]

H460 xenografts were implanted into the subcutaneous space of NOD scid gamma mice. Mice were treated with Milciclib (30 mg kg−1 in 0.5% carboxymethylcellulose; PO; BID), and 24 h after the first treatment, imaged again with 18F-FDG PET. Milciclib blocked glucose consumption in H460 cell xenografts by 30.4 ± 2.5% (pre-treatment and post-treatment).

Measured endpoints — not treatment concentrations
EndpointReported resultReference
glucose consumption in H460 cell xenograftsglucose consumption 30.4 ± 2.5%[3]

Conditions shared by the study groups

Route
PO
Treatment course
BID
Vehicle
0.5% carboxymethylcellulose
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Milciclib 30 mg kg−1pre-treatmentMilciclib (30 mg kg−1 in 0.5% carboxymethylcellulose; PO; BID): 24 h after the first treatment, Milciclib blocked glucose consumption in H460 cell xenografts by 30.4 ± 2.5%, as assessed using 18F-FDG PET imaging (pre-treatment and post-treatment).[3]
Milciclib 30 mg kg−1
Model: H460 xenografts were implanted into the subcutaneous space of NOD scid gamma mice
Methods and source locations

Compound reported in the paper: Milciclib

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

Results > Milciclib inhibits glucose consumption in H460 cells (S52); Methods > 18F-FDG PET (S175, S176, S177); Methods > Statistical analyses (S232); Fig. 3 legend (S246)

glucose consumption in H460 cell xenografts: glucose consumption in H460 cell xenografts; comparator: pre-treatment — Results > Milciclib inhibits glucose consumption in H460 cells (S52); Methods > 18F-FDG PET (S177); Fig. 3 legend (S246)

Milciclib 30 mg kg−1 · Results > Milciclib inhibits glucose consumption in H460 cells (S52); Methods > 18F-FDG PET (S177); Fig. 3 legend (S246)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 802539-81-7
Applications CDK Inhibitor
Formula C25H32N8O
Molecular Weight 460.6
Synonyms PHA848125
SMILES
CC1(CC2=CN=C(N=C2C3=C1C(=NN3C)C(=O)NC)NC4=CC=C(C=C4)N5CCN(CC5)C)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 91 mg/mL (197.58 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.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
30% propylene glycol, 5% Tween 80, 65% D5W

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] Bolin S, Borgenvik A, Persson CU, et al. Combined BET bromodomain and CDK2 inhibition in MYC-driven medulloblastoma. Oncogene (2018). PMID: 29511348 DOI: 10.1038/s41388-018-0135-1 Source material
  2. [2] Ma J, Wu S, Yang X, et al. Milciclib-mediated CDK2 inhibition to boost radiotherapy sensitivity in colorectal cancer. Front Pharmacol (2025). PMID: 40201697 DOI: 10.3389/fphar.2025.1557925 Source material
  3. [3] Ghezzi C, Wong A, Chen BY, et al. A high-throughput screen identifies that CDK7 activates glucose consumption in lung cancer cells. Nat Commun (2019). PMID: 31784510 DOI: 10.1038/s41467-019-13334-8 Source material

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