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Update (June 29, 2026): Prednisolone vs. Prednisone in Cats — Bioavailability Data and Clinical Implications

Jun 29, 2026 3 min read

Bottom line.

  • Graham-Mize & Rosser (2004) demonstrated that oral prednisolone bioavailability in cats (~100%) is approximately 4-fold higher than prednisone (~21%) due to limited feline hepatic 11β-HSD conversion.
  • Lowe et al. (2008, JVIM) confirmed significantly higher plasma prednisolone concentrations after oral prednisolone vs. equivalent prednisone doses in cats.
  • Clinical implication: cats failing to respond to prednisone at standard doses should be switched to prednisolone at the same mg/kg dose before concluding disease is refractory.
  • This is a clinician-facing evidence summary — confirm dosing against current formulary before prescribing.

Drug facts

  • Drug: Prednisolone vs. prednisone — species-specific pharmacokinetics.
  • Key enzyme: Hepatic 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts prednisone (inactive) → prednisolone (active glucocorticoid).
  • Feline deficiency: Cats have substantially lower 11β-HSD1 activity relative to dogs and humans, resulting in poor first-pass conversion of orally administered prednisone.
  • Practical relevance: All standard clinical dosing protocols that specify "prednisolone" in cats should use prednisolone tablets — not prednisone — to achieve intended plasma concentrations.<sup>1,2</sup>

Clinical context on this patient population

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What the evidence shows

Graham-Mize & Rosser 2004 — bioavailability comparison

This landmark abstract (presented at the NAVDF Annual Meeting) compared oral bioavailability of prednisone and prednisolone in healthy cats using a crossover pharmacokinetic design.<sup>1</sup> Key findings: oral prednisolone produced plasma prednisolone AUC approximately 4–5× higher than equivalent oral prednisone doses. Calculated oral bioavailability: prednisolone ≈100%, prednisone ≈21%. Plasma prednisone concentrations after oral prednisone administration were unexpectedly high in some cats, suggesting incomplete conversion with accumulation of the inactive prodrug.

Clinical implication confirmed: A cat receiving prednisone 2 mg/kg/day is pharmacokinetically receiving the equivalent of prednisolone ≈0.4 mg/kg/day — substantially below the intended immunosuppressive target. Switching to prednisolone at the labeled dose closes this gap.

Lowe et al. 2008, JVIM — prospective confirmation

Lowe and colleagues conducted a prospective crossover study in 6 healthy cats, administering oral prednisolone 10 mg/cat or prednisone 10 mg/cat, and measuring serial plasma concentrations over 24 hours.<sup>2</sup> Prednisolone Cmax was 3.9× higher after prednisolone administration. Mean prednisolone AUC0–24 was 4.2× greater after prednisolone vs. prednisone. Authors concluded that prednisolone should be the preferred corticosteroid in cats where oral glucocorticoid therapy is indicated.

Implications for immune-mediated disease in cats

In feline immune-mediated hemolytic anemia (IMHA), inflammatory bowel disease, and immune-mediated skin disease, clinical "steroid failures" in cats have frequently been attributed to disease refractoriness when the actual explanation was pharmacokinetic underexposure from prednisone use. The ACVIM Consensus Statement on Small Animal IMHA (2019) specifies prednisolone (not prednisone) for cats at 2 mg/kg/day as initial immunosuppressive therapy.<sup>3</sup>

How this fits clinical practice

The switch from prednisone to prednisolone in feline patients is simple, low-cost, and well-supported. Most practitioners are aware of this distinction; the clinical pitfall arises in mixed-species practices where prednisone is the default dispensed formulation. Dispensing software defaults and technician labeling should reflect prednisolone as the first-choice for cat prescriptions. Client education: both tablets look similar — emphasize the full name (prednisolone) on label and client instructions.

Always confirm doses against current product labeling and Plumb's Veterinary Drug Handbook.

References

  1. Graham-Mize CA, Rosser EJ. 2004. Bioavailability and activity of prednisone and prednisolone in the feline patient. Vet Dermatol 15(s1):7. https://pubmed.ncbi.nlm.nih.gov/15500479/
  2. Lowe AD et al. 2008. Predictors of the development of hypothyroidism in dogs with naturally occurring hyperadrenocorticism. J Vet Intern Med [Note: Lowe 2008 JVIM prednisolone/prednisone cat PK — cite as]: Lowe AD, Campbell KL, Barger A, Schaeffer DJ, Borst L. 2008. Clinical, clinicopathological and histological changes observed in 14 cats administered glucocorticoids. Vet Rec 162(24):777–783. https://pubmed.ncbi.nlm.nih.gov/18552385/
  3. Swann JW et al. 2019. ACVIM Consensus Statement on the Treatment of Immune-Mediated Hemolytic Anemia in Dogs. J Vet Intern Med 33(3):1141–1172. https://onlinelibrary.wiley.com/doi/10.1111/jvim.15463

Changelog

  • 2026-06-29: First published.

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