Glucocorticoids (GCs) and the Glucocorticoid Receptor (GR): Mechanisms, Classification Frameworks, and the Latest Advances (with a Product Selection Table)

What are glucocorticoids?

Glucocorticoids (GCs) are a class of steroid hormones synthesized in the adrenal cortex from cholesterol, produced mainly in the zona fasciculata. In humans, the predominant endogenous glucocorticoid is cortisol (with corticosterone usually lower), whereas in rats/mice corticosterone is the main glucocorticoid.

Common point of confusion:

“Corticosteroids” is a broader umbrella term that typically includes:

1.Glucocorticoids (GCs): primarily metabolic regulation + anti-inflammatory/immunomodulatory effects + stress adaptation

2.Mineralocorticoids (e.g., aldosterone): primarily electrolyte/fluid balance and blood pressure regulation (mainly controlled by the RAAS and serum potassium; ACTH can provide short-term stimulation, but long-term control is still dominated by RAAS/potassium.)

What are the “typical features” of glucocorticoids?

Think of them as “chemical signals that can cross membranes.” The typical features of glucocorticoids (GCs) can be summarized in four sentences:

1.Lipophilic: Free GCs can cross cell membranes and bind the glucocorticoid receptor (GR) inside cells. Classic effects are largely mediated by regulation of gene expression (though some rapid, non-genomic effects can also occur).

2.Broad actions but highly context-dependent: Most tissues can respond. GCs participate in metabolic homeostasis, stress adaptation, and inflammatory/immune regulation, but the magnitude and direction of effects depend strongly on tissue/cell context and co-regulatory networks.

3.Rhythmicity + negative feedback: The hypothalamic–pituitary–adrenal (HPA) axis drives circadian rhythms and increases GC levels during stress, while negative feedback restrains upstream signaling to prevent runaway responses. Cortisol also shows ultradian (pulsatile) secretion.

4.High clinical value—but dose determines the “cost”: Potent anti-inflammatory/immunosuppressive actions make GCs highly valuable therapeutically; however, systemic adverse effects are strongly related to dose and duration (and route of administration). Common risks include metabolic abnormalities, osteoporosis/fractures, increased infection risk, and HPA-axis suppression.

Where do glucocorticoids act—and what are they “doing” in each domain?

A. Physiology: Why does the body need them?

1.Stress response and energy mobilization: During infection/inflammation/fasting/psychological stress, GCs help maintain glucose supply and mobilize energy; they also exert “permissive/maintenance” effects on vascular reactivity and circulatory homeostasis.

2.Braking inflammation and immunity: Through GR, GCs reshape inflammatory gene networks (e.g., suppressing NF-κB, AP-1 pathways), pulling immune responses back from “runaway amplification” into a controllable range, and promoting resolution of inflammation.

3.Everyday homeostasis: GCs also support routine homeostasis under circadian control—they are not only “called into action” during acute stress.

B. Medicine and pharmacy: Why are they “super commonly used drugs”?

Synthetic glucocorticoids are widely used across disciplines (allergy/asthma, rheumatology/immunology, dermatology, transplantation, hematology/oncology supportive regimens, critical care, etc.). The core reason is that GR-mediated transcriptional regulation powerfully suppresses inflammatory programs. In addition, multiple administration routes (local and systemic) make it possible in many scenarios to achieve “greater target-organ benefit with minimized systemic side effects.”

What is the glucocorticoid receptor GR (glucocorticoid receptor)?

GR is the principal receptor mediating glucocorticoid actions. It is an intracellular, ligand-dependent transcriptional regulator belonging to the nuclear receptor superfamily. The human gene is NR3C1 (nuclear receptor subfamily 3 group C member 1).

How does GR work? (A 4-step “cytoplasm-to-nucleus” sequence)

1.In the absence of hormone: GR is mainly cytoplasmic, associated with a chaperone complex (e.g., Hsp90/Hsp70 heat shock proteins; and FKBP51/52, FK506-binding proteins) and remains in an activatable state (it can also shuttle between nucleus and cytoplasm to some extent).

2.Hormone enters the cell and binds GR: Binding induces conformational changes and triggers chaperone rearrangement.

3.GR translocates to the nucleus: In the nucleus, GR can directly bind GREs (glucocorticoid response elements), or regulate networks such as NF-κB and AP-1 via tethering.

4.Gene-expression networks are remodeled: GR can both upregulate and downregulate transcription, with outcomes strongly dependent on cell type and chromatin context.

Structurally, GR typically consists of an N-terminal transactivation domain (NTD/AF-1), a DNA-binding domain (DBD, with zinc fingers), a hinge region, and a ligand-binding domain (LBD/AF-2).

A useful analogy: the hormone is the key and GR is the lock—but once unlocked, GR goes on to “rewrite the switch states” of a large set of genes.

Note: Molecular chaperones are “protein assistants” that help receptors maintain proper conformation and complete assembly/transport; FKBP51/52 are co-chaperones.

GR is crucial: a “master valve” for many diseases and drug effects

There are three main reasons:

1.Nearly all therapeutic glucocorticoid effects ultimately depend on GR (and its downstream network).

2.The same dose can be highly effective in some people but cause strong side effects in others, which relates to GR-associated mechanisms (receptor isoforms, chaperones, metabolic enzymes, co-regulators, etc.); in practice, we still lack reliable pre-treatment predictors.

3.Glucocorticoid resistance is a major clinical and research problem (e.g., in some asthma, inflammatory diseases, certain tumors/immune states), often involving multiple layers within the GR signaling cascade.

How can GR be “classified”?

Classification axis	Subtype/option	One-line definition	Key details / common pitfalls
1. By receptor itself (isoforms)	GRα (glucocorticoid receptor alpha)	The canonical dominant form: binds glucocorticoids and mediates most classic effects	Not a single protein form: even within GRα, alternative translation initiation can yield multiple N-terminal variants (often referred to as GR-A/B/C/D in the literature), which may differ in activity spectra and gene selectivity—so “GRα” can still show strong tissue differences
	GRβ (glucocorticoid receptor beta)	Produced by alternative splicing; generally thought not to bind conventional glucocorticoids, and can negatively regulate GRα in some contexts (dominant-negative)	Pitfall: treating GRβ only as a “brake.” In some models, GRβ may also have GRα-independent functions (highly context-dependent)
	Other GR isoforms	Beyond α/β, NR3C1 can generate other splice/translation-start combinations (often named GRγ, GR-P, etc. in reviews)	“GR is not just α/β”
2. By signaling output mode (signaling modes)	Genomic actions	After nuclear entry, GR regulates transcription—most systematic and central mode	Three typical “nuclear landing routes”: (1) direct binding to GREs; (2) tethering to inflammatory transcription factors such as NF-κB and AP-1; (3) downregulation via negative regulatory elements (e.g., nGRE, negative GRE)
	Non-genomic actions	Faster (seconds–minutes) effects via membrane/cytoplasmic interactions that influence signaling pathways	Can occur in many contexts; mechanisms may involve membrane-initiated signaling, ion channels/kinase cascades, and rapid processes involving the classical receptor
3. By pharmacological modulation (pharmacological regulation)	Agonists (most clinical therapies)	Activate GR to reshape inflammatory/immune and metabolic networks (strong efficacy)	Real-world key point: broad action spectrum → side effects also come from being “too broad”; “systemic vs local delivery” (inhaled/topical/intra-articular, etc.) strongly shifts the risk–benefit balance
	Antagonists / blockers	Block GR signaling for situations where cortisol effects need to be reduced (e.g., strategies related to Cushing syndrome)	More specialized pathway; indications and monitoring requirements are stricter
	Selective GR modulators (SEGRMs/SEGRAs)	Goal: improve the therapeutic index—retain key efficacy while reducing some adverse effects	Separating efficacy from side effects is not equivalent to the old simplistic dichotomy “transactivation = side effects, transrepression = efficacy”; it is better viewed as distinct gene-regulatory spectra/co-regulator recruitment profiles and biased signaling

Common research or application scenarios

Scenario (research/application)	What it is typically “doing”	Common readouts/methods (research)	Key considerations
Physiology / stress biology (HPA axis)	During stress/inflammation/fasting: coordinates energy and immune responses; uses negative feedback to restore homeostasis	Cortisol/ACTH dynamics; GR nuclear translocation; transcriptomic changes	“Homeostasis maintenance + stress peaks” belong to one integrated system; timing matters
Inflammation & immunology basic research	GR reshapes inflammatory gene networks: suppresses excessive inflammation and promotes resolution/convergence	ChIP-seq/ATAC-seq; GRE reporter assays; interactions/tethering with NF-κB/AP-1	Not simply “turning off immunity”—it’s network remodeling; strong cell-type dependence
Respiratory: asthma/COPD (ICS as a core therapy)	Suppresses airway inflammation, improves symptoms and reduces exacerbations; a major research focus is steroid insensitivity/resistance	Airway-cell GR/HDAC2; cytokine profiles; clinical endotype stratification	“Steroid resistance” spans multiple layers (GR isoforms, chromatin, oxidative stress, etc.)
Rheumatology/autoimmunity (RA, SLE, vasculitis, etc.)	Rapidly suppresses inflammatory “peaks,” bridging until immunomodulators/biologics take effect	Inflammation scores, CRP; dose-tapering trials; target-organ assessment	Benefit vs risk depends strongly on dose/duration/route (local vs systemic)
Dermatology / ophthalmology / ENT (topical, eye drops, nasal sprays)	Suppresses local inflammation while minimizing systemic exposure	Local symptom scales; skin barrier/corneal metrics	“High local potency + low systemic exposure” is a common logic (but long-term use still requires caution)
Transplantation / allergy & immunosuppression regimens	Suppresses rejection/allergic cascades as one component of multi-drug regimens	Immune-cell profiling; rejection markers; infection monitoring	The core long-term tension is balancing immunosuppression with infection risk
Oncology & hematology (“supportive therapy + GR biology in some cancers”)	Regimen support (antiemetic/anti-allergy/anti-inflammatory/anti-edema, etc.); GR is also studied in tumor cell fate and drug resistance in some contexts	Apoptosis/transcriptomics; combination studies with chemo/immunotherapy	The same pathway can be beneficial or harmful depending on tumor type and context—interpretation must be cancer-specific and scenario-specific
Endocrinology: Cushing syndrome (hypercortisolism) and pharmacologic counteraction	Use GR antagonism/modulation to reduce “excess cortisol effects” such as hypertension/hyperglycemia	Clinical endpoints (BP/glucose metabolism/symptoms); safety monitoring	Representative direction: selective GR modulators (e.g., clinical studies of relacorilant)
Neuropsychiatry / stress-related disease research	Study phenotypes linked to excessive GR activation; explore more “precise” interventions	Animal stress models; brain-region-specific multi-omics; GR-related gene regulation	Emerging tool direction: GR degraders such as PROTACs to “turn down” overly strong GR signaling
Drug development: improving therapeutic index	Aim to “retain anti-inflammatory benefits while reducing metabolic/bone side effects”	Co-regulator recruitment profiles; tissue selectivity; long-term safety models	Consensus: no longer equivalent to the old “transactivation = side effects / transrepression = efficacy” dichotomy—mechanisms are more complex
A representative case of “decoupling side effects”	Clinical translation of “decoupled/selective” steroids/modulators	Clinical benefit vs adverse bone/glucose metabolic effects	Example: vamorolone (Agamree) as a representative “selective/decoupled” steroid has received FDA approval (DMD)

Abbreviations

1.HPA axis = hypothalamic–pituitary–adrenal axis

2.GRE = glucocorticoid response element

3.NF-κB = nuclear factor kappa B

4.AP-1 = activator protein-1

5.SEGRMs/SEGRAs = selective GR modulators/agonists

6.PROTAC = proteolysis-targeting chimera

Latest Research Advances

Level	Directional takeaway	Representative points/examples	Why it matters
Mechanistic	GR is no longer viewed as a “simple nuclear on/off switch”	New structural & biophysical picture: elucidating GR conformations, inter-domain communication, and how chaperones (Hsp90/Hsp70, etc.) coordinately regulate GR maturation/activation—helping explain “why the same ligand can yield different transcriptional programs.”	Moves “same drug, different efficacy/side effects” from a phenomenon-level observation toward mechanism: differences may arise from conformational and complex-dynamics states.
	A classic question is still evolving: monomer/dimer/higher-order states	Oligomerization/conformational states are being updated: 2025 work discusses relationships between GR oligomeric conformations and function, indicating the long-standing “monomer vs dimer vs higher-order forms” question is still being refined.	Impacts how we interpret the sources of “transcriptional regulation modes / dose effects / cell-type differences.”
	The evidence chain linking “isoforms → individual differences” is becoming more systematic	GRα/GRβ and additional isoforms (alternative splicing, alternative translation start sites, etc.) are being more systematically organized, helping explain tissue specificity and inter-individual differences/resistance.	Provides a more citable, actionable mechanistic framework for “individual variability / glucocorticoid resistance.”
Pharmacology	Moving from “agonist/antagonist” toward “selective modulation + new tool modalities”	Clinical translation of selective/‘decoupled’ steroids: vamorolone has received FDA approval for DMD and is viewed as a milestone toward improving benefit–risk.	Demonstrates that “selective/decoupled” is not just a concept—real-world translation is beginning to emerge.
	New SEGRMs/SGRMs continue to appear (mostly early-stage)	GRM-01 (2025): animal models suggest an exploratory direction of separating anti-inflammatory efficacy from adverse effects on glucose/bone metabolism (still early/Phase 1–leaning).	Signals that the direction is advancing, but evidence level must be stated cautiously (early-stage/animal).
	Cushing syndrome: clinical evidence continues to accumulate	relacorilant: includes Phase 3 and extension studies; Phase 3 (GRACE/GRADIENT) and long-term extension studies have reported evidence for improvements in clinical endpoints such as hypertension and glycemic metabolism; regulatory approval should follow official final conclusions.	Represents a practical clinical pathway for “blocking/modulating excessive cortisol effects” that continues to strengthen.
	A new route: “not antagonism, but degradation”	GR PROTAC degraders (Nature Communications 2023): as research tools/potential therapeutic concepts, representing a new toolchain.	Expands the toolbox from “modulating activity” to “directly removing the receptor.”
Disease	Glucocorticoid resistance and precision stratification are increasingly emphasized	Severe asthma steroid insensitivity/resistance remains a core challenge; reviews emphasize individualized stratification and summarize multi-layer mechanisms.	Reframes “why some patients don’t respond” from a single-target issue to a “stratification + multi-node network” issue.
	Genetic variation–phenotype links continue to emerge	Ongoing association studies between NR3C1 variants and asthma severity/control (effects depend on cohort and phenotype definitions).	Reminder: such findings may help explain differences, but over-extrapolation should be avoided.

Major Bottlenecks

Bottleneck	Core reason (why it’s hard)	What it means for R&D / clinical practice / research
It is difficult to fully decouple efficacy from side effects	The old dichotomy (“transactivation = side effects / transrepression = efficacy”) is weakening; reality looks more like GR selectively reshaping networks under different tissue/chromatin/co-regulator contexts.	Designing an SEGRM that is “perfect for everyone” is very hard; the same molecule may show different benefit–risk profiles across tissues.
Large inter-individual variability & lack of pre-treatment predictors	Influenced by many factors—GR isoform ratios, chaperones/co-regulators, local metabolism, epigenetics, etc.—yet stable, generalizable predictive systems are lacking.	In practice, it is hard to predict upfront who will benefit more and who will be more prone to side effects; trial-and-error costs are high.
Glucocorticoid resistance/insensitivity remains a long-standing pain point	In severe asthma/chronic airway inflammation, resistance involves oxidative stress, chromatin regulation (e.g., HDAC2-related pathways), and multi-step GR signaling imbalance; single-point fixes are often insufficient.	Requires “stratification + combination intervention/multi-target” thinking; a single mechanism is often not enough.
No robust unified framework for rapid non-genomic effects	Rapid effects (seconds–minutes) are established, but receptor localization, membrane-related mechanisms, and tissue contributions are complex.	“How to leverage/avoid rapid effects” is still hard to engineer; conclusions can vary across models.

Representative Product Selection Table Related to Glucocorticoids & Receptors

(GR/MR tool compounds × systemic/benchmark & soluble forms × local formulations/sustained-release)

First decide what you’re doing, then choose the table:

1.To validate GR/MR pathways, run agonist/antagonist controls, or dissect mechanisms → see Table 1 (Receptor tools)

2.For quantification/QC, building systemic “benchmark controls,” or when water-soluble/injectable forms are needed for dosing/addition → see Table 2 (Systemic & benchmarks)

3.For local therapy/local models (airway, nasal, ocular surface, skin) or when focusing on “local retention/prodrugs/sustained release/formulation forms” → see Table 3 (Local & formulations)

Table 1 | Receptor Tool Compounds: GR/MR Modulation, Antagonism, and Probes (Mechanistic Validation / Pathway Dissection)

Category	CAS No.	Aladdin Cat. No.	Name	Specification / Purity	Product application or highlights
Glucocorticoid receptor-related | GR modulation/antagonism	1496510-51-0	R669597	Relacorilant	Moligand™, ≥98%	Selective GR modulator/antagonist-direction small molecule; for GR pathway blockade, resistance/metabolic-effect studies, and controls.
Glucocorticoid receptor-related | GR antagonist	2222344-98-9	O648769	ORIC-101	≥99%	GR antagonist-direction small molecule; commonly used for GR blockade, combination-mechanism studies, and “anti-glucocorticoid” pharmacology controls.
Glucocorticoid receptor-related | Selective GR modulator	1018679-79-2	C171679	CORT-108297	≥97%	Tool compound in the selective GR modulator direction; used to differentiate downstream GR pathways (e.g., transactivation vs transrepression) in mechanistic studies.
Glucocorticoid receptor-related | High-affinity GR agonist (research probe)	1110-40-3	C667938	Cortivazol	_	Ultra-high-affinity GR agonist probe; for receptor binding/occupancy, signal amplification, and mechanistic validation experiments.
Glucocorticoid receptor-related | GR modulation/antagonism	1496508-34-9	D649407	Dazucorilant	_	GR modulator/antagonist-direction small molecule; used for “anti-glucocorticoid effects,” stress/metabolism-related pharmacology, and mechanistic controls.
Glucocorticoid receptor-related | GR (also PR) antagonist	84371-65-3	M126999	Mifepristone	Moligand™, ≥98%	Common GR blockade control (also has PR antagonism); used in stress-axis/metabolism and “anti-glucocorticoid effect” mechanism studies.
Glucocorticoid receptor-related | Selective GR agonist (research probe)	74915-64-3	R613329	RU28362	Moligand™	Research-grade selective GR agonist tool compound; for receptor signaling pathways, selectivity, and mechanism-dissection experiments.
Mineralocorticoid receptor-related | GC biosynthetic precursor/metabolic-pathway control	152-58-9	C302974	11-Deoxycortisol / Cortexolone	Moligand™, ≥98%	Mineralocorticoid-like (biased toward MR agonism) control; used for mineralocorticoid/electrolyte-homeostasis models and receptor selectivity studies.
Mineralocorticoid receptor-related | MR agonist	64-85-7	D133972	11-Deoxycorticosterone	Moligand™, ≥97% (HPLC)	Classic steroid control in the MR-agonist direction; often used to distinguish GR vs MR effects and compare receptor pathways.
Mineralocorticoid-like | MR agonist (also GC)	514-36-3	F420036	Fludrocortisone acetate	≥98%	Representative mineralocorticoid-like steroid (prominent MR activity, with some GC activity); used as a control for receptor selectivity and electrolyte-homeostasis studies.

Table 2 | Systemic/Benchmark Glucocorticoids + Standards + Water-Soluble / Injectable Forms

Category	CAS No.	Aladdin Cat. No.	Name	Specification / Purity	Product application or highlights
Analytical standard / reference standard | Glucocorticoid	52-21-1	P129282	Prednisolone acetate	Analytical reference standard	Commonly used for LC/LC-MS quantitative calibration, method development, and QC; can also serve as a control for topical/ophthalmic steroid formulations.
Analytical standard / standard solution | Glucocorticoid	83-43-2	M121766	Methylprednisolone standard solution	Moligand™, analytical standard, 100 ng/µl in Acetonitrile	Pre-made standard solution (in acetonitrile) for direct use in LC/LC-MS calibration curves and recovery/matrix-effect evaluation.
Analytical standard / standard solution | Glucocorticoid	378-44-9	B121764	Betamethasone solution reference material in methanol	Moligand™, analytical standard, 1.00 mg/ml	Pre-made standard solution (in methanol) for rapid quantification, method verification, and inter-batch consistency controls.
Analytical standard | Endogenous glucocorticoid (corticosterone)	50-22-6	C119329	Corticosterone	Moligand™, analytical standard	Dominant GC in rodents (commonly used in HPA-axis/stress research); for quantitative assays and endocrine-model controls.
Endogenous glucocorticoid | Cell-culture grade	50-23-7	H657409	Hydrocortisone	Moligand™, animal-free, low endotoxin, for cell culture, ≥98%	Endogenous “cortisol” control; animal-free/low endotoxin—better suited for cell-culture supplementation of GC signaling or receptor-activation experiments.
Endogenous glucocorticoid | Metabolism/enzymology control	53-06-5	C119445	Cortisone	Moligand™, ≥97%	Requires conversion by 11β-HSD to active cortisol; commonly used as a control for metabolism/enzymology, endocrinology, and receptor studies.
Esterified precursor | Glucocorticoid	50-04-4	C129280	Cortisone acetate	≥98% (HPLC)	Acetate ester (precursor/esterified form); for metabolism/receptor comparisons and formulation controls.
Systemic use | Glucocorticoid	53-03-2	P116562	Prednisone	Moligand™, ≥98%	Classic systemic GC prodrug; for in vivo anti-inflammatory/immune models and cross-steroid benchmarking.
Systemic use / control | Glucocorticoid	50-24-8	P276607	Prednisolone	≥98%	Classic systemic GC; often used as an in vivo pharmacodynamics control and for comparing solubility/effect differences among its salts/esters.
Systemic use | Glucocorticoid	14484-47-0	D129585	Deflazacort	Moligand™, ≥98% (HPLC)	Representative systemic steroid; for in vivo anti-inflammatory/immunosuppression models and potency comparisons across GCs.
API/GMP raw material | Glucocorticoid	50-02-2	D137736	Dexamethasone	≥98%	Suitable as an experimental control for formulation development and process/quality-research studies.
Water-soluble salt/solution | Glucocorticoid (phosphate)	125-02-0	P1499394	Prednisolone disodium phosphate	Moligand™, 10 mM in Water	Water-soluble phosphate solution for direct dosing/addition in aqueous systems (cell/in vitro); also commonly used as a control for injectable/water-soluble forms.
Water-soluble salt / injectable precursor | Glucocorticoid (phosphate)	2392-39-4	D107196	Dexamethasone sodium phosphate	Moligand™, ≥98%	Highly water-soluble sodium phosphate; suitable for aqueous cell studies and animal dosing; often used as a potent GR agonist/anti-inflammatory benchmark.
Water-soluble salt / injectable precursor | Glucocorticoid (hemisuccinate)	2375-03-3	M168895	6α-Methylprednisolone 21-hemisuccinate sodium salt	≥98%	Water-soluble sodium hemisuccinate (common injectable form); convenient for aqueous preparation and in vivo dosing/rapid-onset controls.
Water-soluble salt / injectable precursor | Glucocorticoid (succinate)	125-04-2	H329245	Hydrocortisone sodium succinate	≥98%	Highly water-soluble sodium succinate; suitable for aqueous systems and rapid animal dosing—controls for “rapidly usable injectable forms.”
Injectable precursor (succinate ester) | Glucocorticoid	2203-97-6	H132728	Hydrocortisone succinate	≥95%	Succinate ester increases water solubility (often paired conceptually with the sodium salt); for injection/aqueous preparation and in vivo dosing controls.
Parent glucocorticoid | Research/control	124-94-7	T129207	Triamcinolone	Moligand™, ≥99%	Parent triamcinolone (non-acetonide); for GC anti-inflammatory controls, SAR comparisons, or derivative/formulation research.

Table 3 | Local-Use Focus (Inhaled/Nasal/Ophthalmic/Topical) + Sustained-Release Injection / Formulation Precursors

Category	CAS No.	Aladdin Cat. No.	Name	Specification / Purity	Product application or highlights
Local sustained-release injection / topical | Medium-potency glucocorticoid	76-25-5	T101294	Triamcinolone acetonide	Moligand™, ≥99%	Representative triamcinolone “acetonide” steroid; often used in topical or local sustained-release injection studies as a control for “longer duration/stronger local effect.”
Local sustained-release injection | Glucocorticoid (long-acting)	5611-51-8	T346633	Triamcinolone hexacetonide	≥98%	Typical long-acting sustained-release (intra-articular/local injection) control; for slow-release kinetics and arthritis/local inflammation model benchmarking.
Inhaled / nasal | Glucocorticoid	5534-09-8	B129370	Beclomethasone dipropionate	Moligand™, ≥98% (HPLC)	Classic inhaled/nasal steroid; dipropionate increases lipophilicity and local action—suitable for respiratory local anti-inflammatory controls.
Inhaled / nasal | Prodrug-type glucocorticoid	126544-47-6	C287438	Ciclesonide	Moligand™, ≥98% (HPLC)	Representative inhaled/nasal prodrug (locally activated); for studying “local action/reduced systemic exposure” mechanisms and formulation strategies.
Inhaled / nasal (also local intestinal use) | Glucocorticoid	51333-22-3	B129941	Budesonide	Moligand™, ≥98%	Classic inhaled/nasal steroid; also commonly used as a local anti-inflammatory control in airway/gut models and formulation research.
Inhaled / nasal | Glucocorticoid	80474-14-2	F129894	Fluticasone propionate	Moligand™, ≥97%	Classic inhaled/nasal steroid control; for airway local anti-inflammatory models, formulation, and stability studies.
Inhaled / nasal | Glucocorticoid (long-acting)	397864-44-7	F413479	Fluticasone furoate	Moligand™, ≥98%	High-potency, long-acting inhaled/nasal representative; for comparing airway local action, receptor potency, and retention properties.
Topical / nasal | High-potency glucocorticoid	83919-23-7	M157957	Mometasone furoate	≥98% (HPLC)	Representative potent local steroid (commonly topical/nasal); for high-potency local anti-inflammatory controls and formulation research.
Ophthalmic local | Glucocorticoid (“soft steroid”)	82034-46-6	L129196	Loteprednol etabonate	Moligand™, ≥98% (HPLC)	Representative ophthalmic “soft steroid” (designed for rapid metabolic inactivation); for eye-drop/ocular-surface inflammation models and formulation research.
Ophthalmic local | Glucocorticoid	426-13-1	F138831	Fluorometholone	Moligand™, ≥98% (HPLC)	Common ophthalmic steroid control; for ocular local anti-inflammatory testing, eye-drop formulation screening, and stability studies.
Ophthalmic local | High-potency glucocorticoid	23674-86-4	D129472	Difluprednate	Moligand™, ≥98%	Representative potent fluorinated ophthalmic steroid; for eye-drop formulation / intraocular or ocular-surface inflammation model controls and method development.
Ophthalmic local | Glucocorticoid	49697-38-3	R337073	Rimexolone	Moligand™	Representative ophthalmic steroid; for eye-drop screening, ocular-surface/anterior-segment inflammation models, and control experiments.
Topical dermatologic | Low–medium potency glucocorticoid	638-94-8	D129996	Desonide	Moligand™, ≥99%	Low–medium potency topical steroid control; for skin inflammation models, formulation screening, and permeability/retention evaluation.
Topical dermatologic | Medium potency glucocorticoid (ester)	57524-89-7	H336850	Hydrocortisone 17-valerate	≥99%	Valerate increases lipophilicity and skin retention; for topical formulation, transdermal, and local efficacy controls.
Topical dermatologic | Medium potency glucocorticoid (ester)	13609-67-1	H157369	Hydrocortisone 17-butyrate	≥98% (HPLC)	Representative butyrate ester for topical use; for topical formulation screening, local anti-inflammatory controls, and penetration assessment.
Topical dermatologic | Prodrug-type glucocorticoid	74050-20-7	H648363	Hydrocortisone aceponate (Hydrocortisone aceponate)	_	Prodrug-type topical design (local activation/retention); commonly used for skin inflammation models, formulation, and transdermal evaluation.
Topical dermatologic | Medium potency glucocorticoid (ester)	66734-13-2	A354948	Alclometasone dipropionate	_	Representative esterified topical steroid; for local skin anti-inflammatory controls and formulation screening.
Topical dermatologic | Medium potency glucocorticoid	25122-57-0	C303211	Clobetasone butyrate	≥98%	Medium-potency topical steroid representative; for local anti-inflammatory controls, formulation work, and irritancy/tolerability comparisons.
Topical dermatologic | Prodrug-type glucocorticoid	73771-04-7	P348401	Prednicarbate	Moligand™, ≥99%	Prodrug-type topical design (locally activated / reduced systemic exposure tendency); commonly used for topical formulations and pharmacodynamic controls.
Topical dermatologic | Medium–high potency glucocorticoid	2152-44-5	B123298	Betamethasone 17-valerate	≥98%	Valerate increases lipophilicity and local retention; for topical efficacy, permeation, and formulation-screening controls.
Topical dermatologic | Medium–high potency glucocorticoid (pivalate)	2002-29-1	F486837	Flumetasone pivalate	Moligand™ ≥98%	Pivalate increases lipophilicity and local retention; for topical formulation, permeation/retention, and efficacy control studies.
Skin/mucosal local | Glucocorticoid	152-97-6	F337919	Fluperolone	≥96%	Representative local-use GC; for skin/mucosal local anti-inflammatory controls and related formulation research.
Topical dermatologic | High-potency glucocorticoid	356-12-7	F129893	Fluocinonide	Moligand™, ≥98% (HPLC)	High-potency topical steroid representative; for skin inflammation models, transdermal/retention evaluation, and formulation optimization.
Topical dermatologic | High-potency glucocorticoid (fluocinolone acetonide)	67-73-2	F129244	Fluocinolone acetonide	Moligand™, ≥98%	Typical potent topical glucocorticoid control; commonly used for skin inflammation/immune-response models, topical formulation screening, and “local retention/permeation” comparative studies.
Topical dermatologic | High-potency glucocorticoid	382-67-2	D336852	Desoximetasone	Moligand™, ≥98%	High-potency topical steroid representative; commonly used for topical anti-inflammatory controls, erythema/edema pharmacodynamic models, and formulation screening.
Topical dermatologic | High-potency glucocorticoid	33564-31-7	D337813	Diflorasone diacetate	Moligand™, ≥98%	High-potency “diacetate” topical representative; for formulation strategies to increase lipophilicity/skin retention and efficacy controls.
Topical dermatologic | High-potency glucocorticoid	59198-70-8	D304084	Diflucortolone valerate	≥98%	High-potency “valerate” topical representative; for local anti-inflammatory controls, formulation, and skin retention/permeation research.
Topical dermatologic | High-potency glucocorticoid (di-ester)	5593-20-4	B123297	Betamethasone 17,21-dipropionate	≥97%	Di-ester increases lipophilicity and skin retention; for high-potency topical controls, formulation, and permeation/retention evaluation.
Topical dermatologic | Ultra-high potency glucocorticoid	25122-46-7	C123300	Clobetasol propionate	Moligand™, ≥98%	Ultra-high potency topical steroid representative; for strong anti-inflammatory controls, high-agonism receptor-effect studies, or stringent skin models.
Topical dermatologic | Ultra-high potency glucocorticoid	66852-54-8	H129467	Halobetasol propionate	≥98%	Ultra-high potency topical steroid representative; for strong anti-inflammatory controls, refractory skin models, and receptor-potency ceiling comparisons.
Esterified / lipophilic formulation precursor | Glucocorticoid	1177-87-3	D773875	Dexamethasone acetate	Moligand™, ≥96%	Lipophilic acetate ester; suitable for organic-solvent preparation, local formulations/sustained release, or ophthalmic control studies.
Esterified / local formulation | Glucocorticoid	50-03-3	H102192	Hydrocortisone acetate	≥98%	Acetate ester commonly used for topical/local formulation controls; for formulation screening, stability, and local efficacy studies.
Esterified / formulation precursor | Glucocorticoid	53-36-1	M336197	6α-Methylprednisolone 21-acetate	≥98%	Methylprednisolone acetate; commonly used in formulation/sustained-release strategies, SAR comparisons, and control experiments.

Note: The above are representative Aladdin catalog numbers. For additional specifications, please refer to the product tables at the end of this article or search the official website using the CAS number or product name.

Aladdin: https://www.aladdinsci.com/