Fig. 1 · Structure

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Cortisone acetate

Cat. No. A10239 CAS 50-04-4
In chemical structure, it is a corticosteroid closely related to corticosterone. It is used to treat a variety of ailments and can be administered intravenously, orally, intraarticularly (into a joint), or transcutaneously. Cortisone suppresses the immune system, thus reducing inflammation and attendant pain and swelling at the site of the injury.

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Biological Activity

Bioactivity / Mechanism

Cortisone acetate served as a precursor for cortisol in an oral mouse challenge used to assess glucocorticoid activation. Cortisol generation after the challenge did not differ significantly between young and old wildtype cohorts. This assay does not measure direct glucocorticoid-receptor binding. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

In Vitro Studies

In guinea-pig macrophage-rich cultures, cortisone acetate did not significantly inhibit PGE production at concentrations up to 1 μg/ml during 24 h incubation. High-concentration exposure increased PGE output. The response therefore depends on the model and endpoint; it should not be generalized from other glucocorticoids. [2]

Cortisone acetate did not inhibit macrophage PGE production at lower tested concentrations

Cell-based study · Macrophage-rich peritoneal exudate cultures from male outbred Hartley guinea-pigs; source populations contained 60–80% macrophages. [2]

Cortisone acetate had no significant effect on PGE production at concentrations up to 1 μg/ml. At high concentration the response was stimulatory rather than inhibitory. Other glucocorticoid preparations inhibited PGE output in the same assay. This is an endpoint-specific negative result; conversion to hydrocortisone was suggested as an explanation but was not directly measured.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Prostaglandin E-like activity in culture supernatantqualitative result No significant effect at concentrations up to 1 μg/ml; stimulation at high concentration.[2]

Literature-Reported Treatment Conditions

Treatment concentration
Result reported at concentrations up to 1 μg/ml; Figure 3 includes a high-concentration point at 10,000 ng/ml. No exact stimulation threshold is adopted.
Exposure duration
24 h
Method
Drug added immediately before culture; PGE-like activity measured in supernatant.
Vehicle
Drugs added in Eagle’s MEM (20 μl); cells cultured in MEM with 10% heat-decomplemented fetal calf serum.
Co-treatment
No combination therapy; other steroids were separate comparator preparations.
Reported limits
No cortisone acetate IC50 or ID70 reported. Figure 3 and prose differ on the precise high-concentration stimulation threshold; no exact threshold or curve-derived percentage is adopted.
Methods and source locations

Compound reported in the paper: Cortisone acetate; Compound label in the paper: Cortisyl; Roussel

Evidence concerns the reported cortisone acetate material and model; no Adooq lot validation or equivalence to free cortisone or hydrocortisone acetate is established.

pp. 636–640; Methods/Drugs; steroid results p. 638; Figure 3 and caption p. 639; discussion p. 640

Prostaglandin E-like activity in culture supernatant: Radioimmunoassay reported as PGE₂ weight equivalents. Figure 3: means of 6 replicate samples from 2 separate experiments; no error bars or exact P value supplied for cortisone acetate. — pp. 636–640; Methods/Drugs; steroid results p. 638; Figure 3 and caption p. 639; discussion p. 640

In Vivo Studies

In sensitized CBA mice, cortisone acetate given 24 h before oxazolone recall testing markedly reduced or abolished test-site cell migration and left very little or no epidermal vesication. These findings concern a qualitative skin histology endpoint in a contact-sensitivity model. [3]

Age comparison of cortisol generation after an oral cortisone acetate challenge

Animal study · Chow-fed male C57BL/6 wildtype mice in young (12-week) and old (24-month) cohorts defined at euthanasia; cortisone acetate challenge performed 6 weeks before euthanasia. [1]

Cortisol generated after oral cortisone acetate was used as an in-vivo index of hepatic 11β-HSD1 activity. Figure 1D showed no significant difference between young and old wildtype cohorts. The challenge measures cortisol generation, not glucocorticoid-receptor affinity or an anti-inflammatory efficacy endpoint.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cortisol generated after cortisone acetate challengequalitative result No significant age difference (ns), young WT versus old WT.[1]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Single administration
Treatment course
6 weeks before euthanasia; sample after 20 min
Vehicle
Water
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Young wildtype cohort
0.25 mg in 200 μl
Age comparison against old wildtype cohort; both receive challenge.Cortisol generated; no significant difference from old WT.[1]
Old wildtype cohort
0.25 mg in 200 μl
Young wildtype cohort receiving the same challenge.No significant age-associated change in challenge cortisol.[1]
Young wildtype cohort
Model: Chow-fed male C57BL/6 wildtype mice in young (12-week) and old (24-month) cohorts defined at euthanasia; cortisone acetate challenge performed 6 weeks before euthanasia.
Reported limits: No vehicle-only arm shown in Figure 1D.
Old wildtype cohort
Model: Chow-fed male C57BL/6 wildtype mice in young (12-week) and old (24-month) cohorts defined at euthanasia; cortisone acetate challenge performed 6 weeks before euthanasia.
Reported limits: No exact means or P value reported in the adopted text.
Methods and source locations

Compound reported in the paper: Cortisone acetate; Compound label in the paper: Cortisone acetate challenge

Evidence concerns the reported cortisone acetate material and model; no Adooq lot validation or equivalence to free cortisone or hydrocortisone acetate is established.

Design and methods: Mouse ageing protocol, Cortisone acetate challenge and cortisol generation after gavage, Statistical analysis; Results first glucocorticoid-metabolism paragraph; Figure 1D and caption

Cortisol generated after cortisone acetate challenge: GC/MS at 20 min after gavage; unpaired Student’s t-test. Figure 1 caption reports n = 8–9 animals per group; data presented as mean ± SEM. No exact means or P value transcribed from bars. — Design and methods: Mouse ageing protocol, Cortisone acetate challenge and cortisol generation after gavage, Statistical analysis; Results first glucocorticoid-metabolism paragraph; Figure 1D and caption

Young wildtype cohort · Design and methods: Mouse ageing protocol, Cortisone acetate challenge and cortisol generation after gavage, Statistical analysis; Results first glucocorticoid-metabolism paragraph; Figure 1D and caption

Old wildtype cohort · Design and methods: Mouse ageing protocol, Cortisone acetate challenge and cortisol generation after gavage, Statistical analysis; Results first glucocorticoid-metabolism paragraph; Figure 1D and caption

Reduced skin cellular response during oxazolone recall

Animal study · 3–4-month-old CBA mice sensitized to oxazolone and tested for recall on day 10; sex not specified in the shared animal methods. [3]

Compared with sensitized mice not receiving cortisone acetate, administration 24 h before recall testing abolished or markedly reduced cell migration to the test site and produced very little or no epidermal vesication. The outcome is qualitative histology; the study does not establish a molecular receptor mechanism.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Dermal cell infiltration and epidermal vesication after recall testingqualitative result Cell migration abolished or drastically reduced; very little or no epidermal vesication.[3]
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Group E: cortisone acetate before recall
40 mg/100 g body weight
Group D: sensitized and recall-tested without cortisone acetateAbolished or drastically reduced test-site cell migration; very little or no vesication.[3]
Group D: recall without cortisone acetateGroup E receives cortisone acetate on day 9.Polymorph migration to dermis, vesicle formation and lymphocytes at test site.[3]
Group E: cortisone acetate before recall
Model: 3–4-month-old CBA mice sensitized to oxazolone and tested for recall on day 10; sex not specified in the shared animal methods.
Route: Subcutaneous, two sites
Frequency: Single dose
Treatment course: Day 9 after sensitization, 24 h before day-10 test
Reported limits: Vehicle not specified; qualitative small-group histology.
Group D: recall without cortisone acetate
Model: 3–4-month-old CBA mice sensitized to oxazolone and tested for recall on day 10; sex not specified in the shared animal methods.
Treatment course: Day-10 recall test; samples 4, 24 and 48 h later
Reported limits: No vehicle injection described; no numeric scoring.
Methods and source locations

Compound reported in the paper: Cortisone acetate; Compound label in the paper: Adreson; Organon Laboratories

Evidence concerns the reported cortisone acetate material and model; no Adooq lot validation or equivalence to free cortisone or hydrocortisone acetate is established.

p. 674 shared methods; Table 2 p. 675; Results “Effect of cortisone acetate on recall (groups D and E)” pp. 679 and 682

Dermal cell infiltration and epidermal vesication after recall testing: Ear-skin histology using haematoxylin/eosin and methyl-green/pyronin. Table 2: one animal at 4 h, three at 24 h, one at 48 h after testing in each of groups D and E; these are animals, not replicates of a quantitative score. — p. 674 shared methods; Table 2 p. 675; Results “Effect of cortisone acetate on recall (groups D and E)” pp. 679 and 682

Group E: cortisone acetate before recall · p. 674 shared methods; Table 2 p. 675; Results “Effect of cortisone acetate on recall (groups D and E)” pp. 679 and 682

Group D: recall without cortisone acetate · p. 674 shared methods; Table 2 p. 675; Results “Effect of cortisone acetate on recall (groups D and E)” pp. 679 and 682

Specifications

Manufacturer Adooq Bioscience
CAS Number 50-04-4
Formula C23H30O6
Molecular Weight 402.48
Synonyms 17-hydroxy-11-dehydrocorticosterone
SMILES
CC(=O)OCC(=O)[C@]1(CC[C@@H]2[C@@]1(CC(=O)[C@H]3[C@H]2CCC4=CC(=O)CC[C@]34C)C)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 6 mg/mL (14.91 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Morgan SA, Gathercole LL, Hassan-Smith ZK, et al. 11β-HSD1 contributes to age-related metabolic decline in male mice. The Journal of endocrinology (2022). PMID: 36205523 DOI: 10.1530/joe-22-0169 Source material
  2. [2] Bray MA, Gordon D. Prostaglandin production by macrophages and the effect of anti-inflammatory drugs. British journal of pharmacology (1978). PMID: 687875 DOI: 10.1111/j.1476-5381.1978.tb17276.x Source material
  3. [3] De Sousa M, Fachet J. The cellular basis of the mechanism of action of cortisone acetate on contact sensitivity to oxazolone in the mouse. Clinical and experimental immunology (1972). PMID: 5034248 Source material

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