2. GPCR/G Protein Neuronal Signaling Membrane Transporter/Ion Channel Metabolic Enzyme/Protease Immunology/Inflammation NF-κB
  3. Adrenergic Receptor Calcium Channel Potassium Channel Reactive Oxygen Species (ROS)
  4. Landiolol

Landiolol (ONO1101) is a highly selective, ultra-short-acting competitive inhibitor of β1 adrenergic receptors. Landiolol specifically blocks cardiac β1 receptors, reducing heart rate and myocardial oxygen consumption. Landiolol inhibits TNF-α-induced excessive mitochondrial oxygen consumption and reactive oxygen species production in a sepsis model, alleviating renal injury. Landiolol has little effect on cardiac ion channels (such as L-type calcium current and inward rectifier potassium current) and has a weak negative inotropic effect. Landiolol can be used for perioperative tachycardia control and protection studies of sepsis-related acute kidney injury.

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

Landiolol Chemical Structure

Landiolol Chemical Structure

CAS No. : 133242-30-5

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Landiolol Related Antibodies

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N-type calcium channel L-type calcium channel P/Q-type calcium channel T-type calcium channel Calcium Channel

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Description

Landiolol (ONO1101) is a highly selective, ultra-short-acting competitive inhibitor of β1 adrenergic receptors. Landiolol specifically blocks cardiac β1 receptors, reducing heart rate and myocardial oxygen consumption. Landiolol inhibits TNF-α-induced excessive mitochondrial oxygen consumption and reactive oxygen species production in a sepsis model, alleviating renal injury. Landiolol has little effect on cardiac ion channels (such as L-type calcium current and inward rectifier potassium current) and has a weak negative inotropic effect. Landiolol can be used for perioperative tachycardia control and protection studies of sepsis-related acute kidney injury[1][2][3].

IC50 & Target

Beta-1 adrenergic receptor

 

L-type calcium channel

 

IrK

 

In Vitro

Landiolol (10 μM; 24 h) significantly inhibits the increase in mitochondrial oxygen consumption rate (OCR) induced by TNF-α (0.5 nM) in HEK293 cells, reducing the basal OCR from 123% to 94.8%, and reduces the generation of reactive oxygen species (ROS)[1].
Landiolol (10 μM; 24 h) inhibits the excessive glycolytic capacity of HEK293 cells induced by TNF-α (0.5 nM), but does not significantly affect its basal glycolytic (ECAR) level[1].

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

Landiolol Related Antibodies

Cell Viability Assay[1]

Cell Line: HEK293 cells
Concentration: 10 μM (Landiolol)
Incubation Time: 24 h; with 0.5 nM TNF-α
Result: Resulted in a significant reduction in basal OCR compared to TNF-α alone. The OCR, normalized to control (100%), decreased from 123.9%±16.6% (TNF-α only) to 94.8%±13.3% (TNF-α + Landiolol).
Attenuated maximal OCR and ATP production, indicating inhibition of mitochondrial hyperactivity.
Significantly lowered intracellular ROS levels, measured via dichlorodihydrofluorescein (DCF) assay.
In Vivo

Landiolol (0.1 mg/kg/min; intravenous infusion; single dose; 6 h) significantly reduces serum creatinine and lactate concentrations and alleviates renal tubular necrosis and inflammatory damage in the lipopolysaccharide (LPS)-induced acute kidney injury model in rats. Landiolol may not mediate renal protection through systemic anti-inflammatory or antioxidant effects[2].
Landiolol has less effect on cardiac function than Esmolol (HY-B1392A) and does not directly shorten the action potential duration (APD)[3].

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

Animal Model: LPS-induced Acute Kidney Injury Rat Model (250-300 g，6-8 weeks old)[2]
Dosage: 0.1 mg/kg/min
Administration: Continuous intravenous infusion starting at the time of LPS administration (7.5 mg/kg, iv), maintained for 6 h
Result: Significantly improved renal function compared to the LPS group.
Decreased serum creatinine levels to 0.7 ± 0.3 mg/mL versus 1.4 ± 0.7 mg/mL in the LPS group, and decreased lactate levels to 3.8 ± 0.7 mmol/L versus 6.5 ± 1.3 mmol/L, at 6 h.
Reduced tubular degeneration, dilation, and acute necrosis in the renal cortex and medulla in the landiolol group compared to the LPS group.
Urinary 8-OHdG, a marker of oxidative stress, was increased in both groups but not significantly different between them, indicating landiolol’s renoprotection was not mediated by systemic anti-inflammatory or antioxidant effects.
Clinical Trial
Molecular Weight

509.59

Formula

C25H39N3O8
CAS No.
SMILES

O=C(OC[C@H]1OC(C)(C)OC1)CCC2=CC=C(OC[C@@H](O)CNCCNC(N3CCOCC3)=O)C=C2
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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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Landiolol Related Classifications

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Help & FAQs
  • 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:

Landiolol133242-30-5ONO1101ONO 1101ONO-1101Adrenergic ReceptorCalcium ChannelPotassium ChannelReactive Oxygen Species (ROS)Beta ReceptorCa2+ channelsCa channelsKcsAInhibitorinhibitorinhibit

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