| Field | Specification |
|---|---|
| Target | |
| Alternative names | Loprinone Hydrochloride |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C14H11ClN4O |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Olprinone Hydrochloride, also known as Loprinone Hydrochloride, is a potent, selective phosphodiesterase 3 (PDE3) inhibitor, with IC50 values of 150, 100, 0.35, and 14 μM against PDE1, PDE2, PDE3, and PDE4, respectively. It exerts broad protective effects, including anti-inflammatory, antioxidant, and anti-apoptotic activity, by elevating intracellular cAMP levels and inhibiting the NF-κB and MAPK signaling pathways. It can be used in studies related to lung injury, spinal cord injury, myocardial ischemia-reperfusion injury, and cerebral ischemic injury[1][2][3][4][5][6]. It is supplied as a white to off-white solid (C14H11ClN4O, MW 286.72) at 99.85% purity.
Physical & Chemical Properties
| CAS Number | 119615-63-3 |
|---|---|
| Molecular Formula | C14H11ClN4O |
| Molecular Weight | 286.72 g/mol |
| Purity | 99.85% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | CC(N1)=C(C=C(C#N)C1=O)C2=CN3C(C=C2)=NC=C3.[H]Cl |
| Target | PDE1, PDE2, PDE3, PDE4 |
| Signaling Pathway | Metabolic Enzyme/Protease; Apoptosis; NF-κB; MAPK/ERK Pathway |
| Solubility | In Vitro: H2O: ≥ 7.69 mg/mL (26.82 mM) * "≥" means soluble, but saturation unknown. |
| Storage | 4°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
PDE1 150 μM (IC50) |
PDE2 100 μM (IC50) |
PDE3 0.35 μM (IC50) |
PDE4 14 μM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| H2O | ≥ 7.69 mg/mL (26.82 mM) | — |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
If water is used as the stock solvent, dilute to the working solution and sterilize it through a 0.22 μm filter before use.
Data provided by the manufacturer.
In Vitro
In isolated rat alveolar macrophages, Olprinone (Loprinone) hydrochloride hydrate (10 mM; 48-72 h) suppresses LPS-induced production of TNF-α and IL-6 and promotes IL-10 production[2].
ELISA Assay[2]
| Cell Line | Primary rat alveolar macrophages |
|---|---|
| Concentration | 10 mM |
| Incubation Time | 48, 72 h |
| Result | Significantly suppressed the levels of TNF-α and IL-6 at 48 h and 72 h. Augmented the production of IL-10 at 48 h and 72 h. |
In Vivo
In LPS-induced acute lung injury rat models, Olprinone (Loprinone) hydrochloride hydrate (0.2 mg/kg; i.p.; single administration; observation for 6 h) has anti-inflammatory effects and decreases pulmonary neutrophil infiltration[2]. In a mouse model of spinal cord injury, Olprinone (Loprinone) hydrochloride hydrate (0.2 mg/kg; i.p.; given at 1 h and 6 h post-injury, then daily until day 9 post-injury; observation for 10 days) reduces spinal cord inflammation and cell apoptosis and improves hindlimb motor function[3]. In a rabbit model of acute lung injury induced by meconium aspiration syndrome, Olprinone (Loprinone) hydrochloride hydrate (0.2 mg/kg; i.v.; single administration; observation for 5 h) relieves pulmonary oxidative stress and reduces pulmonary edema and inflammatory cell infiltration[4]. In a rat model of myocardial ischemic injury, Olprinone (Loprinone) hydrochloride hydrate (0.2 mg/kg; i.p.; single administration) decreases myocardial infarction size and has anti-inflammatory and anti-apoptotic effects[5]. In a rat model of cerebral ischemia/reperfusion injury, Olprinone (Loprinone) hydrochloride hydrate (0.2 mg/kg; i.p.; single administration; 5 minutes before reperfusion) decreases cerebral infarction volume, improves neurological deficits, and has anti-inflammatory and anti-apoptotic effects[6].
| Animal Model | Wistar rats (male, 180-220 g, acute lung injury model via intravenous Escherichia coli serotype 055:B5 lipopolysaccharide injection at 5 mg/kg)[2] |
|---|---|
| Dosage | 0.2 mg/kg |
| Administration | i.p.; single dose (30 minutes prior to LPS exposure); 6 h |
| Result | Significantly inhibited the LPS-induced neutrophil influx into the lungs. Suppressed inflammatory cytokines TNF-α and IL-6 in the serum. Augmented the production of the anti-inflammatory cytokine IL-10 in the serum. |
| Animal Model | CD1 mice (male adult, 25-30 g, spinal cord injury induced by extradural compression of T5-T8 spinal cord with 24 g closing force for 1 min after four-level T5-T8 laminectomy)[3] |
|---|---|
| Dosage | 0.2 mg/kg |
| Administration | i.p.; 1 h and 6 h post-injury, then daily until day 9 post-injury (motor function assessment); 10 days |
| Result | Reduced the degree of spinal cord inflammation and tissue injury. Attenuated neutrophil infiltration (reduced myeloperoxidase activity) and nitrotyrosine formation. Decreased the expression of pro-inflammatory cytokines (TNF-α, IL-1β) and adhesion molecules (ICAM-1, P-selectin). Inhibited NF-κB expression, p-ERK1/2, and p-p38 MAP kinase activation. Decreased apoptosis, evident by reduced TUNEL staining, Fas ligand, and Bax expression, alongside preserved Bcl-2 expression. Ameliorated the recovery of hind-limb function (BMS score). |
| Animal Model | Chinchilla rabbit (adult, 2.7 kg; meconium aspiration syndrome model via intratracheal meconium instillation)[4] |
|---|---|
| Dosage | 0.2 mg/kg |
| Administration | i.v.; single dose; 5 h |
| Result | Reduced the numbers of neutrophils and eosinophils in the BAL fluid. Decreased the formation of oxidation markers (conjugated dienes, TBARS, dityrosine, and lysine-lipid peroxidation products) in lung mitochondria. Reduced lung edema (decreased wet/dry weight ratio) and prevented a decrease in total antioxidant status (TAS) in the lung homogenate and plasma. Decreased TBARS levels in blood plasma and preserved cytochrome coxidase (COX) activity in the lung. |
| Animal Model | Wistar (male, 270-290 g, transient right hemisphere middle cerebral artery occlusion for 2 hours followed by 22 hours of reperfusion)[6] |
|---|---|
| Dosage | 0.2 mg/kg |
| Administration | i.p.; single dose; 5 minutes before reperfusion |
| Result | Reduced the infarct volume and improved the neurological deficit score. Blocked the acute turning behavior significantly. Suppressed the formation of nitrotyrosine and the expression of iNOS, IL-1β, and ICAM-1 in ischemic tissues. Reduced levels of apoptosis (decreased TUNEL-positive cells and Bax expression, and maintained Bcl-2 expression). |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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bioRxiv. 2024 July 03.
