2. Membrane Transporter/Ion Channel NF-κB Metabolic Enzyme/Protease Immunology/Inflammation Apoptosis
  3. ATP Synthase Reactive Oxygen Species (ROS) Apoptosis Ferroptosis
  4. Antitumor agent-217

Antitumor agent-217 is a dual mitochondria-targeted anticancer agent. Antitumor agent-217 exhibits potent and selective antiproliferative activity against bladder cancer cell line J82 (IC50 = 6.3 μM), and inhibits colony formation and migration of J82 cells. Antitumor agent-217 accumulates in mitochondria, alters mitochondrial morphology, reduces ATP production, increases ROS generation and decreases mitochondrial membrane potential. Antitumor agent-217 induces apoptosis (Apoptosis) and ferroptosis (Ferroptosis) in bladder cancer cells. Antitumor agent-217 can be used for the research of bladder cancer.

For research use only. We do not sell to patients.

Antitumor agent-217

Antitumor agent-217 Chemical Structure

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Antitumor agent-217 Related Antibodies

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Description

Antitumor agent-217 is a dual mitochondria-targeted anticancer agent. Antitumor agent-217 exhibits potent and selective antiproliferative activity against bladder cancer cell line J82 (IC50 = 6.3 μM), and inhibits colony formation and migration of J82 cells. Antitumor agent-217 accumulates in mitochondria, alters mitochondrial morphology, reduces ATP production, increases ROS generation and decreases mitochondrial membrane potential. Antitumor agent-217 induces apoptosis (Apoptosis) and ferroptosis (Ferroptosis) in bladder cancer cells. Antitumor agent-217 can be used for the research of bladder cancer[1].

In Vitro

Antitumor agent-217 (compound 7f) (Range of concentrations; 72 h) inhibits viability of OVCAR3, SKOV3, J82, T24, and A549 cancer cells with highest potency against J82 cells (IC50 = 6.3 μM) and high selectivity over normal SV-HUC-1 cells[1].
Antitumor agent-217 (1.5-6 μM; 6-8 days) dose-dependently inhibits colony formation of J82 bladder cancer cells[1].
Antitumor agent-217 (1.5-6 μM; 24-48 h) dose-dependently inhibits migration of J82 bladder cancer cells[1].
Antitumor agent-217 (10 μM; 4 h) accumulates in mitochondria of J82 bladder cancer cells[1].
Antitumor agent-217 (8 μM; 48 h) disrupts mitochondrial morphology in J82 bladder cancer cells, causing swelling, membrane rupture, and cristae loss[1].
Antitumor agent-217 (2-8 μM, 48 h) dose-dependently reduces ATP production and mitochondrial membrane potential, and increases intracellular ROS levels in J82 bladder cancer cells[1].
Antitumor agent-217 (2-8 μM; 48 h) induces apoptosis in J82 bladder cancer cells at 8 μM by upregulating pro-apoptotic BAX and downregulating anti-apoptotic BCL-2 proteins[1].
Antitumor agent-217 (2-8 μM; 48 h) induces ferroptosis in J82 bladder cancer cells by increasing lipid peroxidation and MDA levels, reducing GSH levels, and downregulating the NRF2/SLC7A11/GPX4 signaling axis[1].

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

Antitumor agent-217 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: J82 human bladder cancer cells
Concentration: 1.5, 3, 6 μM
Incubation Time: 6-8 days
Result: Dose-dependently inhibited colony formation of J82 cells, with significant inhibition at all tested concentrations compared to untreated controls.
Showed slightly greater inhibitory potency than cisplatin at equal concentrations.

Cell Migration Assay [1]

Cell Line: J82 human bladder cancer cells
Concentration: 1.5, 3, 6 μM
Incubation Time: 24 h, 48 h
Result: Significantly reduced the migration ability of J82 cells, with dose-dependent inhibition of wound closure at 24 and 48 h compared to untreated controls.
Exhibited an inhibitory effect comparable to that of cisplatin.

Apoptosis Analysis[1]

Cell Line: J82 human bladder cancer cells
Concentration: 2, 4, 8 μM
Incubation Time: 48 h
Result: Induced 5.02% early apoptosis and 47.5% late apoptosis in J82 cells at 8 μM, with total apoptosis reaching ~52.5%.
Dose-dependently upregulated pro-apoptotic BAX protein and downregulated anti-apoptotic BCL-2 protein, with the BAX/GAPDH ratio increasing to ~1.7 and the BCL-2/GAPDH ratio decreasing to ~0.5 at 8 μM compared to control.
Molecular Weight

668.99

Formula

C32H36BrClN5O2P
SMILES

O=C(OCCC1=CC=CC(/N=C(N)/N=C(N)/N)=C1)CCC[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4.[Br-].Cl
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Antitumor agent-217 Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Antitumor agent-217Antitumor agent217Antitumor agent 217ATP SynthaseReactive Oxygen Species (ROS)ApoptosisFerroptosisSKOV3SV-HUC-1J82ferroptosisOVCAR3bladder cancer cellsmitochondriaapoptosisT24A549Inhibitorinhibitorinhibit

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