H: Systemic hormonal preparations, excluding sex hormones and insulins

ATC group H for modelers: replacement versus pharmacological dosing, the assay that cannot tell drug from hormone, and turnover as the default structure.
Modified

September 22, 2026

Corticosteroids, thyroid therapy and the pituitary and hypothalamic hormones. Sex hormones sit in group G and insulins in group A, so what remains is mainly H01 to H03.

On 21 September 1948 at the Mayo Clinic, Charles Slocumb gave a woman crippled by rheumatoid arthritis 100 mg of Kendall’s “compound E” (now known as cortisone), and within three days she was markedly improved. Hench, Kendall and Reichstein shared the 1950 Nobel Prize [1].

Table 1: ATC H level 2 codes
Level 2 code Description In plain terms Example drug
H01 Pituitary and hypothalamic hormones and analogues hormones of the brain’s master glands Somatropin (H01AC01) / desmopressin (H01BA02)
H02 Corticosteroids for systemic use Prednisolone (H02AB06) / dexamethasone (H02AB02)
H03 Thyroid therapy Levothyroxine sodium (H03AA01) / thiamazole (H03BB02)
H04 Pancreatic hormones pancreas hormones; here glucagon only, not insulin Glucagon (H04AA01) / dasiglucagon (H04AA02)
H05 Calcium homeostasis keeping blood calcium and parathyroid hormone balanced Teriparatide (H05AA02) / cinacalcet (H05BX01)

Modeling notes

The assay cannot tell drug from hormone. Where the agent is the natural hormone, as with thyroxine and hydrocortisone, the model needs an explicit baseline or suppression step rather than a plain PK structure [2,3].

Two regimes, two problems. Replacement restores physiological concentrations and is judged on a feedback biomarker, thyrotropin [4], or for glucocorticoids on clinical assessment with no equivalent marker [5]. Pharmacological dosing deliberately overshoots to exploit an effect the hormone does not produce at normal concentrations [6,7].

Typical structure. Turnover (indirect response), not direct concentration-effect [8,9], with a feedback term when the axis itself is modeled [10] (see PKPD). Steroid and thyroid effects run through nuclear receptors and gene transcription [11], so response lags concentration and shows hysteresis [12].

References

[1]
Matteson EL, Hunder G. Philip S hench and the discovery of cortisone. Annals of the Rheumatic Diseases 2024;83:700–5. https://doi.org/10.1136/ard-2024-225823.
[2]
Walter-Sack I et al. Assessment of levothyroxine sodium bioavailability: Recommendations for an improved methodology based on the pooled analysis of eight identically designed trials with 396 drug exposures. Clinical Pharmacokinetics 2004;43:1037–53. https://doi.org/10.2165/00003088-200443140-00006.
[3]
Melin J et al. Predicting cortisol exposure from paediatric hydrocortisone formulation using a semi-mechanistic pharmacokinetic model established in healthy adults. Clinical Pharmacokinetics 2018;57:515–27. https://doi.org/10.1007/s40262-017-0575-8.
[4]
Chaker L, Bianco AC, Jonklaas J, Peeters RP. Hypothyroidism. The Lancet 2017;390:1550–62. https://doi.org/10.1016/S0140-6736(17)30703-1.
[5]
Janssen Daalen JM et al. Model-informed precision dosing using machine learning for levothyroxine in general practice: Development, validation and clinical simulation trial. Clinical Pharmacology & Therapeutics 2024;116:824–33. https://doi.org/10.1002/cpt.3293.
[6]
Simon N et al. Pharmacokinetic evidence for suboptimal treatment of adrenal insufficiency with currently available hydrocortisone tablets. Clinical Pharmacokinetics 2010;49:455–63. https://doi.org/10.2165/11531290-000000000-00000.
[7]
Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clinical Pharmacokinetics 2005;44:61–98. https://doi.org/10.2165/00003088-200544010-00003.
[8]
Dayneka NL, Garg V, Jusko WJ. Comparison of four basic models of indirect pharmacodynamic responses. Journal of Pharmacokinetics and Biopharmaceutics 1993;21:457–78. https://doi.org/10.1007/BF01061691.
[9]
Lönnebo A, Grahnén A, Karlsson MO. An integrated model for the effect of budesonide on ACTH and cortisol in healthy volunteers. British Journal of Clinical Pharmacology 2007;64:125–32. https://doi.org/10.1111/j.1365-2125.2007.02867.x.
[10]
Bindellini D, Michelet R, Aulin LBS, Melin J, Neumann U, Blankenstein O, et al. A quantitative modeling framework to understand the physiology of the hypothalamic-pituitary-adrenal axis and interaction with cortisol replacement therapy. Journal of Pharmacokinetics and Pharmacodynamics 2024. https://doi.org/10.1007/s10928-024-09934-7.
[11]
Hollenberg SM, Weinberger C, Ong ES, Cerelli G, Oro A, Lebo R, et al. Primary structure and expression of a functional human glucocorticoid receptor cDNA. Nature 1985. https://doi.org/10.1038/318635a0.
[12]
Ramakrishnan R, DuBois DC, Almon RR, Pyszczynski NA, Jusko WJ. Fifth-generation model for corticosteroid pharmacodynamics: Application to steady-state receptor down-regulation and enzyme induction patterns during seven-day continuous infusion of methylprednisolone in rats. Journal of Pharmacokinetics and Pharmacodynamics 2002. https://doi.org/10.1023/a:1015765201129.