Cat. No.: HY-107631

Oxprenoate potassium

Name: Oxprenoate potassium
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(Synonyms: RU 28318)

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Oxprenoate (RU 28318) potassium is an orally active, brain-penetrant selective mineralocorticoid receptor antagonist that blocks Aldosterone (HY-113313) signaling through competitive binding to MR, and exhibits anxiolytic and neuroprotective activities, as well as modulates Corticosterone (HY-B1618) levels. Oxprenoate potassium is used in research on hypertension, anxiety disorders, depression, Alzheimer's disease, and glucocorticoid-related neuronal injury.

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Pureté : 98.05%
CAS No.: 76676-34-1
Formule: C₂₅H₃₇KO₄
Masse moléculaire:440.66

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* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Oxprenoate potassium Chemical Structure

CAS No.: 76676-34-1

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Description

In Vitro

Oxprenoate (RU 28318) is a potent mineralocorticoid receptor antagonist that attenuates aldosterone-induced upregulation of γENaC mRNA in acute rat hypothalamic slices containing the PVN and SON, with no independent effect on the basal expression of any ENaC subunit mRNA^[8].
Oxprenoate (120 min) blocks the increase in Ouabain (HY-B1457)-dependent ²²Na efflux stimulated by Aldosterone (HY-113313)^[9].

Oxprenoate (1 μM; 60 minutes) has no detectable effect on baseline electrophysiological action potential parameters, APD₉₀ dispersion, or the incidence of spontaneous premature ventricular contractions in an isolated rabbit right ventricular ischemia-reperfusion border zone model^[7].
Oxprenoate (1 μM) does not alter the baseline open probability of the endogenous 30 pS IK1 potassium channel in freshly isolated rabbit ventricular cardiomyocytes^[7].
Oxprenoate (20 h) is a selective type I receptor ligand, and no activity against type II receptors is detected in cell-free hippocampal cytosol adrenosteroid receptor binding assays^[1].
Oxprenoate (5 μM; 3 days) does not alter basal ¹²⁵I-NGF binding in wtPC12 cells^[4].
Oxprenoate (5 μM; 3 days) has no effect on baseline catecholamine levels in wtPC12 cells^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

In Vivo

Oxprenoate (RU 28318) (1-5 ng; bilateral intrahippocampal microinjection) produces significant anxiolytic effects in intact male Long-Evans rats in the elevated plus maze test and defensive burying test, whereas the 5 ng dose has no such effect^[2].
Oxprenoate (0.2-0.5 ng; bilateral intrahippocampal microinjection) induced anxiolytic effect in the elevated plus maze is completely abolished by adrenalectomy, indicating that endogenous corticosterone is necessary for its anxiolytic action^[2].
Oxprenoate (0.2-1 ng; bilateral intrahippocampal microinjection) induced anxiolytic effect in the open field thigmotaxis test and elevated plus maze test are completely blocked by systemic pretreatment with 80 μg/kg Dexamethasone (HY-14648), confirming that intact endogenous corticosterone signaling is a prerequisite for its efficacy^[2].
Oxprenoate (10 μg/μl/hr; i.c.v.; continuous infusion via osmotic minipump; for 6 consecutive days) completely prevents DOCA-induced anhedonia by maintaining baseline LHSS ECu₅₀ values, whereas acute central administration of Oxprenoate further decreases ECu₅₀ to enhance reward responsiveness in Male Sprague-Dawley rats (250-375 g) subjected to a DOCA-induced chronic non-remitting appetite model^[6].
Oxprenoate (10 μg/μl/hr; i.c.v. and s.c.; delivered continuously via osmotic minipump for 12 days) significantly suppresses DOCA-induced salt appetite in Sprague-Dawley male rats (250-375 g) with DOCA-induced chronic salt appetite, when administered centrally (but not peripherally)^[6].
Oxprenoate (administered orally 1 h before subcutaneous aldosterone injection) is a mineralocorticoid antagonist that dose-dependently blocks aldosterone-stimulated ²²Na efflux in rat vascular smooth muscle, with greater potency in inhibiting the ouabain-dependent efflux mediated by the sodium pump^[9].
Oxprenoate (compound MR) (100 mg/kg; p.o.) prevents the stress-induced increase in exploratory attempts, improves locomotor behavior, enhances rearing activity, lowers blood glucose levels, and elevates plasma CORT levels in rats subjected to acute and chronic restraint stress^[3].
Oxprenoate (100 mg/kg; p.o.) reverses CORT-induced motor impairment, reduces the number of attempted grasps in rats, improves motor component scores, increases vertical exploratory rearing activity, and lowers blood glucose levels in rats with long-term exposure to exogenous corticosterone^[3].
Oxprenoate (compound A-MR) (100 ng/2 µl; i.c.v.; single infusion 15 min before restraint) abolishes the stress-induced anxiogenic-like effects in rats without altering spontaneous locomotor activity levels^[10].
Oxprenoate (10 mg/kg; s.c.; twice daily for 3 days) does not alter ethanol preference, water intake, or total fluid intake in adrenalectomized rats implanted with corticosterone or in sham-operated intact rats^[5].
Oxprenoate (50 mg/kg; s.c.) achieves approximately 85% type I receptor occupancy in the hippocampus, blocks aldosterone-mediated enhancement of long-term potentiation (LTP), and does not cause significant changes in basal LTP or neuronal excitability in adrenalectomized rats^[1].

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

Animal Model:

Long-Evans rats (adult male, weighing 300-400 g at experiment time, implanted with bilateral cannulae aimed 2 mm above the hippocampal dentate gyrus)^[4]
Dosage:

1 ng; 5 ng
Administration:

bilateral intrahippocampal microinjection; infused at 0.25 μL per minute, injection cannula left in place for 1 minute per side after infusion
Result:

Exhibit 12.3 open arm entries, 10.8 closed arm entries, 128.3 seconds of time spent in open arms, and 103.0 seconds of time spent in closed arms at 1 ng dose in the elevated plus-maze, representing a significant increase in open arm entries and open arm time, and significant decrease in closed arm time relative to the vehicle control group.
Increase the latency to initiation of burying behavior and reduce total duration of time spent burying the electrified probe at 1 ng dose in the defensive burying test.
Show no changes in any of the elevated plus-maze or defensive burying behavioral measures at 5 ng dose.

Animal Model:

Long-Evans rats (adult male, weighing 300-400 g at experiment time, underwent adrenalectomy or sham surgery, implanted with bilateral hippocampal cannulae)^[4]
Dosage:

0.2 ng; 0.5 ng
Administration:

bilateral intrahippocampal microinjection; infused at 0.25 μL per minute, injection cannula left in place for 1 minute per side after infusion
Result:

Produce 14.4 open arm entries, 15.8 closed arm entries, 47.8% of total arm entries that were open entries, 193 seconds of time spent in open arms, 171 seconds of time spent in closed arms, and 52.5% of total time spent in open arms at 0.5 ng dose in sham-operated animals, representing an 80 second increase in total open arm time relative to the sham vehicle control value of 113 seconds, and a 100 second decrease in total closed arm time relative to the sham vehicle control value of 271 seconds, generating a significant anxiolytic effect.
Show no anxiolytic effects in adrenalectomized animals at 0.2 ng or 0.5 ng dose.

Animal Model:

Long-Evans rats (adult male, weighing 300-400 g at experiment time, implanted with bilateral hippocampal cannulae, randomly assigned to receive either systemic dexamethasone 80 μg/kg or vehicle pretreatment to suppress endogenous glucocorticoid secretion)^[4]
Dosage:

0.2 ng; 0.5 ng; 1 ng
Administration:

bilateral intrahippocampal microinjection; infused at 0.25 μL per minute, injection cannula left in place for 1 minute per side after infusion
Result:

Decrease thigmotaxis time in the open field at 0.5 ng dose in vehicle-pretreated animals.
Increase the proportion of time spent on the open arms in the elevated plus-maze at 0.5 ng and 1 ng doses in vehicle-pretreated animals.
Show fully blocked anxiolytic effects at 0.5 ng and 1 ng doses in dexamethasone-pretreated animals.
Exhibit a significant anxiogenic effect at 0.5 ng dose in dexamethasone-pretreated animals.

Animal Model:

Long-Evans rats (adult male, weighing 300-400 g at experiment time, implanted with bilateral hippocampal cannulae, randomly assigned to receive either systemic dexamethasone or vehicle pretreatment, evaluated for serum corticosterone levels before, immediately after, and 90 minutes after a 15-minute restraint stress)^[4]
Dosage:

1 ng
Administration:

bilateral intrahippocampal microinjection; infused at 0.25 μL per minute, injection cannula left in place for 1 minute per side after infusion
Result:

Significantly increase basal serum CORT levels.
Maintain significantly elevated serum CORT levels above baseline values 90 minutes following restraint stress in vehicle-pretreated animals, preventing return to the baseline levels observed in vehicle-treated control animals.
Show no such sustained elevation effect in dexamethasone-pretreated animals, where CORT levels 90 minutes post-stress return to baseline.

Animal Model:

Male Sprague-Dawley rats weighing 250-375 g^[8]
Dosage:

10 μg/μl/hr (chronic); single acute central injection
Administration:

i.c.v. (chronic infusion via osmotic minipump); i.c.v. (single acute injection)
Result:

Reduced the elevated ECu50 value of 7.08 observed during DOCA-only phase back to a baseline-matching ECu50 value of 5.66 during the co-administration phase.
Maintained ECu50 at baseline levels (baseline 5.71, phase 1 5.41) when co-administered during initial 6 days of DOCA exposure, preventing the expected DOCA-induced elevation in reward threshold.
Showed no change in ECu50 from baseline in animals treated alone for 12 days, with mean values trending downward from 5.67 at baseline to 4.75 at phase 1 and 4.61 at phase 2.
Decreased ECu50 relative to baseline after acute administration, reducing the value from 5.89 to 4.03, indicating enhanced responsiveness to lateral hypothalamic self-stimulation reward.
Caused no changes in maximum responses per minute (RPM) for any chronically treated group, confirming no motor impairment in lever pressing behavior.

Animal Model:

Male Sprague-Dawley rats weighing 250-375 g^[8]
Dosage:

10 μg/μl/h
Administration:

i.c.v. or s.c. (chronic infusion via osmotic minipump; 12 consecutive days)
Result:

Significantly reduced DOCA-induced 0.3 M saline intake when delivered via intracerebroventricular route, with treated animals consuming less saline than all other comparison groups on day 3, day 5, and days 6 through 11 of the 12-day treatment period.
Did not reduce DOCA-stimulated 0.3 M saline intake when delivered via subcutaneous route, with subcutaneous-treated rats exhibiting saline intake levels nearly identical to those of the DOCA-only control group across all measured time points.
Caused no changes in daily water intake at any time during the 12-day experiment.

Animal Model:

Long-Evans hooded rats (Adult male and female, 90 days old, weighing 250-300 g (females) and 400-600 g (males))^[5]
Dosage:

100 mg/kg
Administration:

p.o.; 1 h prior to testing on day 1, day 13, and day 14
Result:

Improved reaching success compared to stress-only controls on days 1, 13, and 14, though success rates remained lower than individual baseline performance.
Prevented the stress-induced increase in the number of reaching attempts on day 1 relative to baseline and stress-only controls.
Elevated total movement scores above levels of stress-only controls.
Produced higher grasp, supination I and supination II movement scores than stress-only controls.
Resulted in more rears in exposed male animals after chronic stress compared to stress-only controls.
Lowered blood glucose levels compared to stress-only controls.
Increased plasma CORT concentrations at the chronic exposure time point relative to animals' own baseline levels.

Animal Model:

Long-Evans hooded rats (Adult male and female, 90 days old, weighing 250-300 g (females) and 400-600 g (males))^[5]
Dosage:

100 mg/kg
Administration:

p.o.; 1 h prior to testing on day 1, day 13, and day 14
Result:

Produced higher skilled reaching success rates on days 1, 13, and 14 compared to CORT-only exposed animals.
Reduced the number of reaching attempts compared to CORT-only controls.
Elevated orient, digits close, digits open, and grasp movement scores relative to CORT-only controls.
Resulted in more rears at the chronic CORT exposure time point compared to animals' own baseline and CORT-only control animals.
Lowered blood glucose levels relative to CORT-only controls.

Animal Model:

Wistar rats (adult male, 280-300 g)^[12]
Dosage:

100 ng/2 µl
Administration:

i.c.v.; single infusion 15 min before restraint
Result:

Showed 2.2 open arm entries and 7.3 total arm entries, and prevented the restraint-induced decrease in time spent in the open arms of the elevated plus-maze.
Exhibited no changes in the number of closed arm entries.
Unrestrained rats treated with A-MR spent 18.4% of their time in open arms, a value comparable to unrestrained vehicle-treated controls.
Exhibited elevated basal serum CS levels and showed no serum CS response to restraint stress.

Animal Model:

Wistar rats (male, ~90 days of age at study initiation)^[7]
Dosage:

10 mg/kg
Administration:

s.c.; twice daily; 3 consecutive days
Result:

Yielded a mean ethanol preference of 42.3% of total fluid intake, a mean water intake of 21.3 g/kg/6 h, and a mean total fluid intake of 36.6 g/kg/6 h in adrenalectomized rats bearing corticosterone implants.
Yielded a mean ethanol preference of 35.8% of total fluid intake, a mean water intake of 12.3 g/kg/6 h, and a mean total fluid intake of 19.4 g/kg/6 h in sham-operated adrenally intact rats.
Showed no significant alteration to ethanol preference, water intake, or total fluid intake in either adrenalectomized corticosterone-implanted rats or sham-operated intact rats.

Animal Model:

Sprague-Dawley rats (Male, 250-400 g at the time of testing, bilaterally adrenalectomized 3 days prior to the experiment)^[3]
Dosage:

50 mg/kg
Administration:

s.c. (single injection)
Result:

Produced a population spike LTP of +47.8% relative to baseline when administered alone.
Abolished the aldosterone-induced enhancement of LTP, resulting in a population spike LTP value of +49.1%.
Reduced Type I adrenal steroid receptor binding in hippocampal cytosol to 9.9 fmol/mg protein, representing ~85% occupancy of Type I receptors, while Type II receptor binding was 154.5 fmol/mg protein.
Resulted in Type I receptor binding of 5.6 fmol/mg protein and Type II receptor binding of 142.6 fmol/mg protein when combined with aldosterone.
Did not affect neuronal excitability, the percentage of animals exhibiting post-tetanic potentiation, or EPSP slope LTP outcomes.

Chemical Information

CAS No. 76676-34-1
Appearance Solid
Masse moléculaire 440.66
Formule C₂₅H₃₇KO₄
Color White to off-white
SMILES

CCC[C@H](CC1=CC2=O)[C@@]([C@@](CC3)([H])[C@]1(CC2)C)([H])[C@@](CC[C@](O)4CCC(O[K])=O)([H])[C@@]43C
Synonyms

RU 28318
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Publications (1)

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Cell Metab

Ferroplasticity drives social isolation-induced anxiety via a ventral hippocampal iron-α-synuclein axis. [Abstract]

2026 Jan 27:S1550-4131(25)00586-8. PMID: 41605214

Protocole

All Animals and Diseases Signal Pathway Related

Neurotoxicity Study
This protocol assesses in vitro neurotoxicity by combining neuronal viability, mitochondrial/metabolic activity, neurite outgrowth, and optional neuronal network function readouts. Calcein-AM or resazurin/PrestoBlue readouts estimate viable or metabolically active cells; βIII-tubulin immunofluorescence detects neuronal morphology and neurite networks; TMRE detects mitochondrial membrane potential; and MEA recordings detect functional changes in neuronal network activity.
Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.

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Références

[1]. Pavlides C, et al. Opposing roles of type I and type II adrenal steroid receptors in hippocampal long-term potentiation. Neuroscience. 1995 Sep;68(2):387-94. [Content Brief]

[2]. Bitran D, et al. Corticosterone is permissive to the anxiolytic effect that results from the blockade of hippocampal mineralocorticoid receptors. Pharmacology, biochemistry, and behavior. 1998 Aug;60(4):879-87. [Content Brief]

[3]. Jadavji NM, et al. Blockade of mineralocorticoid and glucocorticoid receptors reverses stress-induced motor impairments. Neuroendocrinology. 2011;94(4):278-90.

[4]. Lazarovici P. Dexamethasone-induced down-regulation of nerve growth factor receptor p75NTR is mediated by glucocorticoid type II receptor in PC12 cell model[J]. The Open Pharmacology Journal, 2007.

[5]. Fahlke C, et al. Consequence of long-term exposure to corticosterone or dexamethasone on ethanol consumption in the adrenalectomized rat, and the effect of type I and type II corticosteroid receptor antagonists. Psychopharmacology. 1995 Jan;117(2):216-24.

[6]. Morris MJ, et al. Mineralocorticoid receptor antagonism prevents hedonic deficits induced by a chronic sodium appetite. Behavioral neuroscience. 2010 Apr;124(2):211-24. [Content Brief]

[7]. Alexandre J, et al. Rapid and MR-Independent IK1 Activation by Aldosterone during Ischemia-Reperfusion. PloS one. 2015;10(7):e0132592.

[8]. Mills NJ, et al. Aldosterone Mediated Regulation of Epithelial Sodium Channel (ENaC) Subunits in the Rat Hypothalamus. Neuroscience. 2018 Oct 15;390:278-292.

[9]. Moura AM, et al. Direct action of aldosterone on transmembrane 22Na efflux from arterial smooth muscle. Rapid and delayed effects. Hypertension. 1984 May-Jun;6(3):425-30.

[10]. Calvo N, et al. Glucocorticoid and mineralocorticoid receptors are involved in the facilitation of anxiety-like response induced by restraint. Neuroendocrinology. 2001 Apr;73(4):261-71.

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Oxprenoate potassium

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Oxprenoate potassium

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