2. Metabolic Enzyme/Protease Apoptosis Epigenetics Cell Cycle/DNA Damage
  3. Pyruvate Carboxylase (PC) Apoptosis Ferroptosis Caspase Bcl-2 Family PARP Glutathione Peroxidase
  4. CIB-Q22

CIB-Q22 is a potent pyruvate carboxylase (PC) inhibitor with an IC50 of 1.74 nM. CIB-Q22 suppresses hepatocellular carcinoma (HCC) cell proliferation, migration, and invasion. CIB-Q22 induces apoptosis and ferroptosis, promotes mitochondrial oxidative stress and dysfunction, inhibits glycolysis and anaplerotic flux, and reverses epithelial-mesenchymal transition (EMT). CIB-Q22 can be used for the study of hepatocellular carcinoma.

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CIB-Q22

CIB-Q22 Chemical Structure

CAS No. : 2963747-43-3

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CIB-Q22 Related Antibodies

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

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PARP PARP1 PARP2 PARP3 PARP4 TNKS1/PARP5A TNKS2/PARP5B PARP7 PARP10 PARP14 PARP15 PARP12 PARP16

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GPX1 GPX4

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Description

CIB-Q22 is a potent pyruvate carboxylase (PC) inhibitor with an IC50 of 1.74 nM. CIB-Q22 suppresses hepatocellular carcinoma (HCC) cell proliferation, migration, and invasion. CIB-Q22 induces apoptosis and ferroptosis, promotes mitochondrial oxidative stress and dysfunction, inhibits glycolysis and anaplerotic flux, and reverses epithelial-mesenchymal transition (EMT). CIB-Q22 can be used for the study of hepatocellular carcinoma[1].

IC50 & Target

Bax

 

Bcl-2

 

Caspase 3

 

GPX4

 

Cellular Effect
Cell Line Type Value Description References
A549 IC50
213.5 nM
Exhibits potent cytotoxicity against A549 cells for 48 h.
Exhibits potent cytotoxicity against A549 cells for 48 h.
42286802
Huh-7 IC50
78.86 nM
Exhibits potent cytotoxicity against Huh-7 cells for 48 h.
Exhibits potent cytotoxicity against Huh-7 cells for 48 h.
42286802
MHCC97L IC50
153.3 nM
Exhibits potent cytotoxicity against MHCC97L cells for 48h.
Exhibits potent cytotoxicity against MHCC97L cells for 48h.
42286802
HCCLM3 IC50
25.18 nM
Exhibits potent cytotoxicity against HCCLM3 cells for 48 h.
Exhibits potent cytotoxicity against HCCLM3 cells for 48 h.
42286802
In Vitro

CIB-Q22 (48 h) exhibits potent cytotoxicity against HCCLM3, Huh-7, MHCC97L, and A549 cells, with IC50 values of 25.18 nM, 78.86 nM, 153.3 nM, and 213.5 nM, respectively[1].
CIB-Q22 (48 h) shows minimal cytotoxicity against SK-Hep-1 cells, which express low levels of PC, as well as against normal RPE-1 cells[1].
CIB-Q22 shows no significant cardiotoxicity in a hERG potassium channel inhibition assay compared to the positive control Terfenadine (HY-B1193)[1].
CIB-Q22 (10-40 nM; 21 days) suppresses the proliferative capacity of HCCLM3 cells [1].
CIB-Q22 (2-10 nM; 24 h) decreases the migration and invasion of HCCLM3 cells, upregulates E-cadherin, and downregulates N-cadherin and fibronectin[1].
CIB-Q22 (40-160 nM; 48 h) induces apoptosis in HCCLM3 cells[1].
CIB-Q22 (50-1600 nM; 52 °C) stabilizes PC thermal stability in HCCLM3 cells in a dose-dependent manner[1].
CIB-Q22 (40-160 nM; 0-48 h) activates Caspase-3 and induces PARP cleavage in HCCLM3 cells in time- and concentration-dependent manners[1].
CIB-Q22 (40-160 nM; 48 h) induces mitochondrial dysfunction in HCCLM3 cells[1].
CIB-Q22 (40-160 nM; 48 h) increases the levels of lipid peroxidation in HCCLM3 cells[1].
CIB-Q22 (40-160 nM; 48 h) induces ferroptosis in HCC cells in a PC-dependent manner[1].
CIB-Q22 (40 nM; 1-6 h) induces a significant increase in intracellular ROS production in HCCLM3 cells[1].
CIB-Q22 (40 nM; 24 h) induces oxidative stress in HCCLM3 cells, as evidenced by reduced NADH/NAD⁺ and GSH/GSSG ratios, decreased ATP levels, and suppressed glucose consumption and lactate production[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

CIB-Q22 Related Antibodies

Western Blot Analysis[1]

Cell Line: HCCLM3 cells
Concentration: 2, 5, or 10 nM
Incubation Time: 24 h
Result: Upregulated E-cadherin and downregulated N-cadherin and fibronectin in HCCLM3 cells.

Western Blot Analysis[1]

Cell Line: HCCLM3 cells
Concentration: 40, 80, or 160 nM
Incubation Time: 0, 2, 4, 12, 24 or 48 h
Result: Activated Caspase-3 and induced PARP cleavage in a time-dependent manner (160 nM; (0, 2, 4, 12, 24 or 48 h). Activated Caspase-3 and induced PARP cleavage in a concentration-dependent manner (40, 80, or 160 nM; 48 h).

Western Blot Analysis[1]

Cell Line: HCCLM3 cells
Concentration: 40, 80, or 160 nM
Incubation Time: 48 h
Result: Downregulated GPX4 and SLC7A11/xCT expression; induced ferroptosis in a PC-dependent manner.

Cell Proliferation Assay[1]

Cell Line: HCCLM3 cells
Concentration: 10, 20, or 40 nM
Incubation Time: 21 days
Result: Suppressed the proliferative capacity of HCCLM3 cells in a concentration-dependent manner.

Cell Invasion Assay[1]

Cell Line: HCCLM3 cells
Concentration: 2, 5, or 10 nM
Incubation Time: 24 h
Result: Decreased the number of invading HCCLM3 cells.

Apoptosis Analysis[1]

Cell Line: HCCLM3 cells
Concentration: 40, 80, or 160 nM
Incubation Time: 48 h
Result: Induced apoptosis in HCCLM3 cells in a concentration-dependent manner.

Immunofluorescence[1]

Cell Line: HCCLM3 cells
Concentration: 40 nM
Incubation Time: 0, 1, 3, or 6 h
Result: Induced a significant increase in intracellular ROS production.
Parmacokinetics
Species Dose Route T1/2 Tmax Cmax AUC0-∞ AUC0-t MRT0-t MRT0-∞ C0 Vss CL Vz F
Mice[1] 10 mg/kg i.v. 1.21 h 0.083 h 5793.9 ng/mL 3062.96 ng·h/mL 3073.17 ng·h/mL 0.69 h 0.72 h 8129.43 ng/mL 239.02 mL/kg 337.77 mL/h/kg 599.15 mL/kg /
Mice[1] 25 mg/kg p.o. 1.79 h 0.33 h 508.67 ng/mL 1060.10 ng·h/mL 1069.27 ng·h/mL 2.49 h 2.62 h / / / / 13.84 %
In Vivo

CIB-Q22 (15-50 mg/kg ; i.p.; every 2 days; 21 days) suppresses tumor growth in an orthotopic HCC mouse model (MHCC97L-luciferase cells in SCID mice) without causing significant body weight changes, exhibiting comparable antitumor efficacy but improved safety compared to Sorafenib (HY-10201) [1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Five-week-old male SCID mice are orthotopically injected with 50 μL of 1 × 106 MHCC97L-luciferase cells into the left liver lobe [1]
Dosage: 15 mg/kg, 30 mg/kg, 50 mg/kg
Administration: Intraperitoneal injection (i.p.); every 2 days; 21 days (starting 7 days after tumor implantation)
Result: Significantly inhibited tumor growth in a dose-dependent manner. Did not cause significant body weight changes at any dose, indicating minimal systemic toxicity. H&E staining of major organs revealed no evident pathological abnormalities, suggesting favorable long-term safety. Immunohistochemical (IHC) analysis of tumor tissues showed significantly reduced GPX4 expression and increased 4-HNE level, a key marker of ferroptosis. TUNEL staining demonstrated increased apoptotic cell death within tumor tissues.
Molecular Weight

335.37

Formula

C18H22FNO4
CAS No.
SMILES

NC1=C(F)C(CCC2=CC(OC)=C(OC)C(OC)=C2)=CC=C1OC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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CIB-Q22 Related Classifications

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Keywords:

CIB-Q222963747-43-3Pyruvate Carboxylase (PC)ApoptosisFerroptosisCaspaseBcl-2 FamilyPARPGlutathione PeroxidasePyruvate Carboxylase poly ADP ribose polymerasePyruvate carboxylase (PC) inhibitorHepatocellular carcinomaHCCHCCLM3Huh-7MHCC97LSK-Hep-1A549apoptosisferroptosisoxidative stressmitochondrial dysfunctionglycolysisglutamine deprivationorthotopic liver tumor modelSCID micesorafenibInhibitorinhibitorinhibit

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