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Fig. 1 · Structure
Cat. No.
A11149
CAS No.
702674-56-4
Formula
C20H23BrN8O
Mol. Weight
471.4

Documents & Downloads

BX-912

Cat. No. A11149 CAS 702674-56-4

PDK1 inhibitor

BX-912 is an inhibitor of 3-Phosphoinositide-dependent Kinase-1 (PDK1).

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Biological Activity

Target & Activity

Target Activity Value
PDK-1 IC50 12nM
PKA IC50 110nM
KDR IC50 410nM
CDK2/CyclinE IC50 650nM
Chk1 IC50 830nM
c-Kit IC50 850nM
PKC IC50 1.25μM
T-Fyn IC50 2.1μM
InsulinReceptor IC50 6.1μM
GSK-3β IC50 7.4μM
EGFR IC50 >10μM

11 targets · Scroll to view more

In Vitro Studies

BX-912 treatment added to OBM decreased the number of ALP-positive cells in BMSCs compared with the control. In chlamydial-infected HeLa cells, BX-912 markedly reduced infection-induced phosphorylated PDPK1 Ser-241 compared with DMSO-treated infected monolayers. In MDA-MB-231 cells, PD-L1 protein expression progressively decreased with increasing BX-912 doses. [1,2,3]

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

Reduced ALP-positive cell counts in BMSCs

Cell-based study · BMSCs [1]

In BMSCs, treatment added to OBM decreased the number of ALP-positive cells compared with the control.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
number of ALP-positive cellsALP-positive cells 25±10/well (0.5 µM)[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.1–0.5 µM
Exposure duration
7 days
Method
added to the OBM
Co-treatment
Other interventions in this design: ascorbic acid 50 µg/ml; sodium β-glycerophosphate 10 mM; dexamethasone 10−7 M. Compound effect isolated by the comparison: vs. Control.
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: BX-912

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

Materials and methods > Untitled > Induction of BMSC differentiation into osteoblasts (S39); Results > Untitled > BX-912 inhibits BMSC differentiation into osteoblasts in vitro (S96, S99); Figure 2. legend (S132, S135); Figure 5. legend (S152)

number of ALP-positive cells: number of ALP-positive cells; comparator: 0 µM — Results > Untitled > BX-912 inhibits BMSC differentiation into osteoblasts in vitro (S99)

Phosphorylated PDPK1 in infected HeLa cells

Cell-based study · HeLa cells [2]

Chlamydial-infected HeLa monolayers were treated with BX-912 or DMSO. BX-912 markedly reduced infection-induced phosphorylation of PDPK1 Ser-241 compared with DMSO-treated infected monolayers.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Western blot showing reduced levels of phosphorylated PDPK1Reported result markedly reduced the degree to which phosphorylated PDPK1 Ser-241 was induced after chlamydial infection[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
12 h p.i. for 36 h
Vehicle
DMSO
Co-treatment
Other interventions in this design: CTL2 MOI 1. Compound effect isolated by the comparison: DMSO-treated and BX912-treated infected monolayers.
Reported limits
Not stated in the sentences used: route.
Methods and source locations

Compound reported in the paper: BX-912

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

Results > PDPK1 is Phosphorylated and Recruited to Chlamydia trachomatis Inclusions (S55); Results > PDPK1 Activation is Required for the Phosphorylation of MYC at Ser-62 and Chlamydial Growth (S68, S69, S71); Fig. 3 legend (S133)

Western blot showing reduced levels of phosphorylated PDPK1: Western blot showing reduced levels of phosphorylated PDPK1; comparator: DMSO-treated — Results > PDPK1 Activation is Required for the Phosphorylation of MYC at Ser-62 and Chlamydial Growth (S69); Fig. 3 legend (S133)

PD-L1 expression in MDA-MB-231 cells

Cell-based study · MDA-MB-231 cells [3]

MDA-MB-231 cells were treated with increasing doses of BX-912. PD-L1 protein expression was progressively inhibited as the dose increased.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
PD-L1 protein levelsReported result PD-L1 expression were progressively inhibited with increasing doses of BX-912[3]

Literature-Reported Treatment Conditions

Exposure duration
24 h
Reported limits
Not stated in the sentences used: dose, route, vehicle, control.
Methods and source locations

Compound reported in the paper: BX-912

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

Results > FTO promotes PD-L1 expression through the PDK1/AKT/STAT3 pathway (S252, S264)

PD-L1 protein levels: PD-L1 protein levels — Results > FTO promotes PD-L1 expression through the PDK1/AKT/STAT3 pathway (S252, S264)

In Vivo Studies

BX-912 was administered by daily gavage to female BALB/c mice bearing cell-derived allografts established with 4 T1 cells. Tumor volume and weight were reduced in the BX-912 treatment group compared with the control group at experiment termination. [3]

Tumor volume and weight in an allograft model

Animal study · female BALB/c; cell-derived allograft (CDA) mice model established with 4 T1 cells; n = 7 [3]

Female BALB/c mice bearing cell-derived allografts established with 4 T1 cells received BX-912 by daily gavage. Tumor volume and weight were reduced in the BX-912 treatment group compared with the control group at experiment termination.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
The volume of the tumor was recorded every 2 daysReported result tumors volume and weight were also reduced in the FB23 or BX-912 treatment group compared with the control group at the termination of the experiment[3]

Conditions shared by the study groups

Route
gavage
Treatment course
daily; for a total of 14 days starting from the 5th day
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
BX-912 1 mg/kgcontrol grouptumors volume and weight were also reduced in the FB23 or BX-912 treatment group compared with the control group at the termination of the experiment[3]
BX-912 1 mg/kg
Model: female BALB/c; cell-derived allograft (CDA) mice model established with 4 T1 cells; n = 7
Reported limits: Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: BX-912

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

Materials and methods > In vivo tumorigenesis and models (S7, S11); Results > Inhibition of FTO enhances the efficacy of anti-PD-L1 therapy in vivo (S272, S274, S286, S300)

The volume of the tumor was recorded every 2 days: The volume of the tumor was recorded every 2 days; comparator: control group — Results > Inhibition of FTO enhances the efficacy of anti-PD-L1 therapy in vivo (S274, S286)

BX-912 1 mg/kg · Materials and methods > In vivo tumorigenesis and models (S11); Results > Inhibition of FTO enhances the efficacy of anti-PD-L1 therapy in vivo (S274)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 702674-56-4
Applications PDK1 inhibitor
Formula C20H23BrN8O
Molecular Weight 471.4
SMILES
C1CCN(C1)C(=O)NC2=CC=CC(=C2)NC3=NC=C(C(=N3)NCCC4=CN=CN4)Br

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 80 mg/mL (169.72 mM)
Water Insoluble
Ethanol 80 mg/mL (169.72 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
28 mg/mL
Vehicle
30% PEG400+0.5% Tween80+5% propylene glycol

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] Bai Y, Zhang Q, Zhou Q, et al. Effects of inhibiting PDK‑1 expression in bone marrow mesenchymal stem cells on osteoblast differentiation in vitro. Mol Med Rep (2021). PMID: 33300048 DOI: 10.3892/mmr.2020.11757 Source material
  2. [2] Al-Zeer MA, Xavier A, Abu Lubad M, et al. Chlamydia trachomatis Prevents Apoptosis Via Activation of PDPK1-MYC and Enhanced Mitochondrial Binding of Hexokinase II. EBioMedicine (2017). PMID: 28803120 DOI: 10.1016/j.ebiom.2017.08.005 Source material
  3. [3] Wang S, Zhang X, Chen Q, et al. FTO activates PD-L1 promotes immunosuppression in breast cancer via the m6A/YTHDF3/PDK1 axis under hypoxic conditions. J Adv Res (2025). PMID: 39701379 DOI: 10.1016/j.jare.2024.12.026 Source material

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