2. Apoptosis Metabolic Enzyme/Protease NF-κB Immunology/Inflammation
  3. Ferroptosis Apoptosis Glutathione Peroxidase ACSL Family Reactive Oxygen Species (ROS) Mitochondrial Metabolism Caspase Bcl-2 Family
  4. Ferroptosis/apoptosis inducer-5

Ferroptosis/apoptosis inducer-5 (Compound 14) is an orally active inducer of Ferroptosis and Apoptosis. Ferroptosis/apoptosis inducer-5 downregulates GPX4, upregulates ACSL4, promotes ROS production, activates the Caspase cascade, induces Mitochondrial dysfunction, and alters the Bcl-2/Bax balance. Ferroptosis/apoptosis inducer-5 significantly inhibits tumor growth in a pancreatic cancer xenograft mouse model. Ferroptosis/apoptosis inducer-5 can be used for the research of pancreatic cancer.

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Ferroptosis/apoptosis inducer-5

Ferroptosis/apoptosis inducer-5 Chemical Structure

CAS No. : 2243423-32-5

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Ferroptosis/apoptosis inducer-5 Related Antibodies

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Description

Ferroptosis/apoptosis inducer-5 (Compound 14) is an orally active inducer of Ferroptosis and Apoptosis. Ferroptosis/apoptosis inducer-5 downregulates GPX4, upregulates ACSL4, promotes ROS production, activates the Caspase cascade, induces Mitochondrial dysfunction, and alters the Bcl-2/Bax balance. Ferroptosis/apoptosis inducer-5 significantly inhibits tumor growth in a pancreatic cancer xenograft mouse model. Ferroptosis/apoptosis inducer-5 can be used for the research of pancreatic cancer[1].

IC50 & Target[1]

Bax

 

Bcl-2

 

GPX4

 

ACSL4

 

In Vitro

Ferroptosis/apoptosis inducer-5 (1.36 μM; 48 h) potently and selectively inhibits the viability of PANC-1 pancreatic cancer cells with an IC50 of 1.36 μM, while showing weaker cytotoxicity against normal 3T3-L1 cells[1].
Ferroptosis/apoptosis inducer-5 (0.5-2.0 μM; 48 h treatment, followed by 10 days of culture without compound) dose-dependently inhibits the long-term colony-forming ability of PANC-1 pancreatic cancer cells, with near-complete suppression at 2.0 μM[1].
Ferroptosis/apoptosis inducer-5 (0.125-2.0 μM; 24 h, 48 h) inhibits the proliferation of PANC-1 pancreatic cancer cells in a concentration- and time-dependent manner, with significant effects observed at 0.25-2.0 μM over 48 h[1].
Ferroptosis/apoptosis inducer-5 (0.125-0.5 μM; 24 h) dose-dependently inhibits the migration and invasive potential of PANC-1 pancreatic cancer cells, with significant effects at 0.5 μM over 24 h[1].
Ferroptosis/apoptosis inducer-5 (0.5-2.0 μM; 48 h) dose-dependently induces G0/G1 phase arrest in PANC-1 pancreatic cancer cells, inhibiting cell proliferation by blocking completion of the replication cycle[1].
Ferroptosis/apoptosis inducer-5 (0.5-2.0 μM; 24 h) dose-dependently increases intracellular ROS levels in PANC-1 pancreatic cancer cells, with significant elevation at 0.5 μM over 24 h[1].
Ferroptosis/apoptosis inducer-5 (0.5-2.0 μM; 48 h) dose-dependently induces apoptosis in PANC-1 pancreatic cancer cells, as evidenced by classical apoptotic morphological changes after 48 h of incubation[1].
Ferroptosis/apoptosis inducer-5 (0.5-2.0 μM; 24 h) activates the intrinsic mitochondrial apoptotic pathway in PANC-1 pancreatic cancer cells by altering Bcl-2/Bax balance, promoting cytochrome c release, and activating the caspase cascade after 24 h of incubation[1].
Ferroptosis/apoptosis inducer-5 (0.5-2.0 μM; 24 h) induces ferroptosis in PANC-1 pancreatic cancer cells by downregulating GPX4 and upregulating ACSL4 after 24 h of incubation[1].

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

Ferroptosis/apoptosis inducer-5 Related Antibodies

Cell Cytotoxicity Assay[1]

Cell Line: human pancreatic cancer PANC-1 cells, human choroidal melanoma C918 cells, mouse embryonic fibroblast 3T3-L1 cells
Concentration: 1.36 μM (PANC-1 IC50); 9.25 μM (3T3-L1 IC50)
Incubation Time: 48 h
Result: Showed potent cytotoxicity against PANC-1 cells with an IC50 of 1.36 μM, far superior to parent betulinic acid (IC50 = 79.29 μM).
Exhibited selective cytotoxicity with an IC50 of 9.25 μM against normal 3T3-L1 cells.
Displayed strong activity against C918 cells.

Cell Proliferation Assay[1]

Cell Line: human pancreatic cancer PANC-1 cells
Concentration: 0.5-2.0 μM
Incubation Time: 48 h treatment, followed by 10 days of culture without compound
Result: Significantly inhibited PANC-1 colony formation in a concentration-dependent manner.
Almost completely suppressed colony formation at 2.0 μM.

Cell Proliferation Assay[1]

Cell Line: human pancreatic cancer PANC-1 cells
Concentration: 0.125-2.0 μM
Incubation Time: 24 h, 48 h
Result: Inhibited PANC-1 cell proliferation in a concentration- and time-dependent manner.
Showed no significant effect at 0.125-0.5 μM over 24 h.
Produced significant inhibition at 0.25-2.0 μM over 48 h.

Cell Cycle Analysis[1]

Cell Line: human pancreatic cancer PANC-1 cells
Concentration: 0.5-2.0 μM
Incubation Time: 48 h
Result: Induced dose-dependent G1 phase arrest in PANC-1 cells.
Increased G1 phase cell percentage.
Decreased S phase cell percentage.
Caused a slight reduction in G2 phase cell percentage.

Apoptosis Analysis[1]

Cell Line: human pancreatic cancer PANC-1 cells
Concentration: 0.5-2.0 μM
Incubation Time: 48 h
Result: Induced a dose-dependent increase in apoptotic PANC-1 cells.
Caused enhanced blue fluorescence (nuclear condensation/fragmentation) and increased red fluorescence (cell membrane integrity loss).

Western Blot Analysis[1]

Cell Line: human pancreatic cancer PANC-1 cells
Concentration: 0.5-2.0 μM
Incubation Time: 24 h
Result: Dose-dependently upregulated pro-apoptotic Bax and cytosolic cytochrome c.
Downregulated anti-apoptotic Bcl-2.
Increased levels of Cleaved-Caspase-9 and Cleaved-Caspase-3.\nDose-dependently downregulated anti-ferroptotic GPX4.
Upregulated pro-ferroptotic ACSL4.
Parmacokinetics
Species Dose Route Tmax Cmax T1/2 AUC0-∞ MRT0-∞
Rat[1] 20 mg/kg p.o. 4.0 h 49.30 μg/mL 5.47 h 337.29 μg·h/mL 7.53 h
In Vivo

Ferroptosis/apoptosis inducer-5 (compound 14) (5-20 mg/kg; i.p.; every 2 days; 28 days) exhibits dose-dependent, significant antitumor activity in a pancreatic cancer xenograft model, achieving a 68.9% tumor weight reduction at the 20 mg/kg dose, while maintaining favorable in vivo safety[1].

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

Animal Model: C57BL/6 (female, 6 weeks old, 17-20 g, SPF grade, subcutaneous xenograft model via Panc02 cell injection)[1]
Dosage: 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: i.p.; every 2 days; 28 days
Result: Reduced tumor weight by 37.1% relative to control.
Reduced tumor weight by 57.0% relative to control.
Reduced tumor weight by 68.9% relative to control, with no significant difference in tumor inhibition rate compared to positive control gemcitabine.
Showed dose-dependent reduction in tumor volume over the 28-day treatment period.
Induced dose-dependent tumor cell apoptosis (increased TUNEL-positive cells), reduced cell proliferation (decreased Ki-67 staining), and downregulated GPX4 expression (indicating ferroptosis induction) in tumor tissues.
Caused no significant pathological abnormalities in heart, liver, spleen, lung, or kidney tissues; serum levels of ALT, AST, BUN, and creatinine were statistically unchanged relative to control.
Molecular Weight

868.01

Formula

C53H72BrO3P
CAS No.
SMILES

O=C(OCCCCC[P+](C1=CC=CC=C1)(C2=CC=CC=C2)C3=CC=CC=C3)[C@@]45CC[C@@]6(C)[C@]7(C)CC[C@@]8([H])C(C)(C)[C@@H](O)CC[C@]8(C)[C@@]7([H])CC[C@]6([H])[C@@]4([H])[C@H](C(C)=C)CC5.[Br-]
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Keywords:

Ferroptosis/apoptosis inducer-52243423-32-5FerroptosisApoptosisGlutathione PeroxidaseACSL FamilyReactive Oxygen Species (ROS)Mitochondrial MetabolismCaspaseBcl-2 FamilyBcl-2Baxapoptosispancreatic cancer xenograft mouse modelsferroptosisGPX4PANC-1 pancreatic cancer cellsACSL4pancreatic cancer3T3-L1 cellsInhibitorinhibitorinhibit

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