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prednisolone

✓ Approved

Takeda · NR3C1 · Small Molecule

What is prednisolone?

prednisolone is a small molecule developed by Takeda. It is approved for therapeutic indications via oral (po).

Drug Profile

CompanyTakeda
Drug ClassSmall Molecule
Molecular TargetNR3C1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Takeda

Mechanism of Action

Molecular Targets

prednisolone acts on 1 molecular target:

NR3C1nuclear receptor subfamily 3 group C member 1 (GR, GCCR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

prednisolone is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Plasma cell myeloma✓ Approved

Related Research Articles

PubMedAnnals of vascular diseases2026-07-17

Asymptomatic Periaortitis Following Endovascular Abdominal Aortic Repair: A Case Report of Spontaneous Resolution with Recurrence and Reactivation during Treatment.

Aiba Masahiro M, Hamaishi Makoto M

A patient who underwent endovascular abdominal aortic repair for a non-inflammatory abdominal aortic aneurysm developed asymptomatic periaortitis 2.5 years postoperatively. Conservative management resulted in aneurysm shrinkage and reduced inflammation. However, at 6 years postoperatively, tumor-like soft tissue shadows appeared around the aorta and the aneurysm diameter re-expanded. This was diagnosed as a recurrence and worsening. Prednisolone was initiated, leading to reductions in both aneurysm size and the mass-like shadow size. When the dosage was decreased, inflammation flared up again. The medication dose was then increased. Gradual dose reduction was subsequently attempted and treatment was successfully discontinued without recurrence.

PMID 42466432
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PubMedClinical case reports2026-07-17

Potential Treatment of Steroid-Resistant Alopecia Areata Using Allogeneic Exosomes Derived From Adipose Tissue Mesenchymal Stromal Cells: A Case Report.

Kianpisheh Masoumeh M, Piroozhashemi Mohsen M, Feshangchian-Atashbar Shabnam S, Ghamari Ali A et al.

A 31-year-old man with severe, corticosteroid-resistant alopecia areata presented with substantial scalp hair loss (Severity of Alopecia Tool [SALT] score: 60%) despite a 1-year regimen of topical corticosteroids, 5% minoxidil, and oral prednisolone. He was treated with allogeneic exosomes derived from adipose tissue mesenchymal stromal cells (ADMSCs-Exo) at 3-week intervals over 12 weeks (four sessions; 1012 particles each). A cessation of hair shedding was noted after the initial session, followed by progressive regrowth that led to near-complete hair restoration by Week 12. Treatment was accompanied by an increase in anti-inflammatory cytokines (IL-4, IL-6, IL-10) and a reduction of IFN-γ, TNF-α, and IL-17 toward baseline levels. No adverse effects were reported during active treatment or throughout the 18-week posttreatment follow-up period. While limited to a single patient, this case suggests that ADMSC-derived exosomes warrant further investigation as a potential cell-free therapeutic option for refractory alopecia areata.

PMID 42466009
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PubMedFrontiers in neurology2026-07-17

Rituximab in Myasthenia Gravis: a real-world study using inverse probability of treatment weighting.

Wang Yong Lin YL, Zhu Chao C, Kapoor Mahima M, Cutter Gary G et al.

The role of rituximab in the treatment of myasthenia gravis (MG) remains uncertain due to limited randomized controlled evidence and heterogeneous observational data. While rituximab is often used in refractory MG, its comparative effectiveness against other non-steroidal immunosuppressive therapies (NSISTs) has yet to be fully clarified. To evaluate the effectiveness of rituximab compared to a second NSIST in achieving a composite clinical outcome in acetylcholine-receptor-antibody (AChR-Ab) positive MG patients using causal inference methods to adjust for confounding. We conducted a retrospective cohort study of AChR-Ab positive MG patients treated with rituximab or a second NSIST. The primary outcome was time to achieving a composite clinical endpoint representing a patient acceptable symptom state (PASS): Myasthenia Gravis Composite (MGC) score ≤ 3, daily corticosteroid dose ≤ 5 mg prednisolone equivalent, and no rescue therapy use in the preceding month. To reduce confounding by indication and improve causal comparability between treatment groups, inverse probability of treatment weighting (IPTW) based on propensity scores was used to balance baseline covariates. Cox proportional hazards models were applied to estimate the effect of treatment on time to outcome. 169 patients entered into the time-to-event analysis, and after IPTW adjustment, baseline characteristics between treatment groups were balanced. There was no statistical difference in the hazard ratio between Rituximab compared to a second NSIST in achieving the composite clinical outcome (HR = 1.27, 95% CI 0.66-2.45, p = 0.48). In this IPTW-adjusted analysis, rituximab did not improve the time-to-improvement compared to a second NSIST in AChR-Ab-positive MG.

PMID 42465546
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PubMedThe Journal of dermatology2026-07-17

Granulomatous Vasculitis in Cutaneous Hydrophilic Polymer Embolism.

Kanaya Moe M, Mitsui Yasuhiro Y, Sasaki Shoh S, Ochi Anna A et al.

Hydrophilic polymers are widely used as coatings on intravascular devices to reduce friction with the vessel wall, thereby minimizing vascular injury and vasospasm. However, delamination of these coatings can lead to hydrophilic polymer embolism (HPE), which may cause distal ischemia and/or inflammation. HPE can involve the brain, skin, heart, kidneys, and lungs, with clinical manifestations varying by sites. Cutaneous findings typically include livedo racemosa and purpuric macules on the lower extremities, emerging hours to days after endovascular procedures. We report a unique case of cutaneous HPE presenting with granulomatous vasculitis. An 82-year-old man presented with a fever of 38°C and painful erythematous macules on his lower limbs. He had undergone endovascular repair of an abdominal aortic aneurysm 22 days earlier. The eruption initially began on the thighs and progressed to involve the lower extremities, resulting in difficulty walking. Skin biopsy revealed angiocentric inflammatory infiltrates from the dermis to the subcutis, with suppurative granuloma formation. Non-polarizing intravascular material was identified within vessels at the dermal-subcutaneous junction, along with features of necrotizing vasculitis. Elastica van Gieson staining highlighted the intravascular materials in purple-black and demonstrated disruption of the internal elastic lamina of the arteriole and small artery. The lesions responded well to oral prednisolone (15 mg/day), which was tapered and discontinued over 2 weeks. Although similar granulomatous features have been described in other organs, to our knowledge, this is the first report of cutaneous HPE with granulomatous vasculitis. This case expands the clinicohistopathological spectrum of cutaneous HPE and alerts dermatologists to HPE as a differential diagnosis of cutaneous granulomatous vasculitis, particularly in patients following endovascular interventions. Notably, cutaneous manifestations may arise weeks after the procedure. Systemic corticosteroids may represent a potential therapeutic option in such cases.

PMID 42466713
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PubMedFrontiers in immunology2026-07-16

Case Report: sustained five-year remission in eosinophilic granulomatosis with polyangiitis with intestinal perforation after surgery and rituximab-based therapy without glucocorticoid escalation.

Yamamura Yuriko Y, Matsumoto Yoshinori Y, Ohashi Keiji K, Hayashi Keigo K et al.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a systemic necrotizing vasculitis characterized by eosinophilic infiltration and granuloma formation, affecting multiple organs. Gastrointestinal (GI) involvement is relatively uncommon and it typically presents with nonspecific symptoms, such as abdominal pain or diarrhea; in contrast, ulceration and intestinal perforation are rare, but potentially life-threatening complications that often require surgical intervention. The standard treatment for severe GI EGPA includes high-dose glucocorticoids combined with cyclophosphamide or rituximab (RTX). However, the perioperative escalation of glucocorticoids is generally avoided owing to the increased risk of postoperative complications. We report a case with a 5-year follow-up of EGPA resistant to multiple immunosuppressive agents with severe GI involvement, including intestinal perforation and multiple jejunal ulcers, which was successfully treated with RTX for postoperative remission induction and long-term maintenance therapy without any prednisolone escalation. The prednisolone dose was gradually reduced from 17.5 mg/day to 1 mg/day over two years without any escalation, and a sustained remission was achieved throughout the course. This case suggests that RTX may represent a viable therapeutic option for severe or treatment-resistant EGPA in cases with GI involvement when glucocorticoid escalation is undesirable or unsafe, such as in the perioperative setting.

PMID 42459667
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PubMedArthritis & rheumatology (Hoboken, N.J.)2026-07-16

A Multi-Center Integrative Cohort Characterizing the Genetic, Clinical, and Transcriptomic Features of ACP5 Deficiency.

Zhong Shiling S, Ma Shuangyue S, El Chazli Yasmine Y, Zheng Jika J et al.

Spondyloenchondrodysplasia with immune dysregulation (SPENCDI) is a rare disorder caused by biallelic mutations in ACP5. This study systematically evaluates genetic landscape, clinical features, treatment, and transcriptomics in SPENCDI. Whole-exome sequencing was performed for genetic diagnosis of patients from multiple centers, and tartrate-resistant acid phosphatase (TRAP) activity was measured for novel variants. Previously reported cases were integrated with the current cohort for analysis of genotypes, clinical characteristics, laboratory findings, and treatment responses. Bulk and single-cell RNA sequencing investigated immune signaling alterations. We identified 17 patients with ACP5 deficiency from Egypt and China, discovering five novel pathogenic variants (A260D, L257P, G32D, K190Nfs*22, and T305Nfs*12). Three novel missense variants were detected with loss of TRAP activity. Clinical manifestations involve multiple systems, with the skeletal system most frequently involved (32.31%), where skeletal dysplasia (94.32%) and short stature (81.82%) are the predominant features. Patients showed elevated inflammatory activity, with enrichment of the NF-κB, MAPK, and cell death pathways, as well as upregulation of type I interferon genes in monocytes. Enhanced IFN-γ signaling interactions between monocytes and Natural Killer cells were observed. Therapeutically, Prednisolone and Azathioprine were the most common effective drugs, while patients treated with the Janus kinase inhibitors Ruxolitinib or Upadacitinib achieved a partial response. This study expanded the genetic and clinical spectrum of ACP5 deficiency. An upregulated interferon signature was revealed, and monocytes were identified as a major cellular source of inflammation. These results provide valuable insights for improving the diagnosis and treatment of SPENCDI.

PMID 42459138
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