The review was published in Frontiers in Pharmacology on 22 October 2026. It is a critical narrative synthesis rather than a prospectively registered systematic review, and its authors searched PubMed, Web of Science, ScienceDirect, CNKI, Wanfang and reference lists through May 2026, followed by a targeted update through 18 August. They grouped evidence by experimental unit: complete-product studies, studies of individual ingredients or defined extracts, and adjacent research on related prescriptions, delivery systems or disease mechanisms. This hierarchy was designed to prevent findings about a purified compound or an authenticated plant material from being presented as proof that the complete capsule works. The review also had no duplicate independent screening, formal risk-of-bias instrument or new quantitative synthesis and therefore did not provide pooled effect estimates or grade certainty.

Within traditional Chinese medicine, ulcerative colitis has no exact one-to-one equivalent, but its symptoms overlap with categories such as dysentery, diarrhea and intestinal wind. The syndrome commonly called intestinal damp-heat describes frequent urgent stools containing mucus or blood, abdominal discomfort, tenesmus and a feeling of incomplete evacuation. The five materials are assigned complementary roles within that framework: Sophora flavescens is the principal heat-clearing and damp-drying ingredient; Sanguisorba officinalis is associated with cooling blood and reducing bleeding; Indigo naturalis is used for heat-clearing and blood-cooling functions; Bletilla striata contributes hemostatic and tissue-repair functions; and licorice is intended to harmonize the combination. These roles generate testable hypotheses, including whether control of bleeding is accompanied by reduced mucosal inflammation, rather than replacing biomedical diagnosis or established measures of disease severity.

The capsule is defined by both its ingredients and its pharmaceutical design. Its enteric coating is intended to protect the contents during passage through the upper gastrointestinal tract and increase delivery to the distal bowel. That design remains a formulation hypothesis rather than a demonstrated exposure profile. Active ulcerative colitis can alter transit and luminal pH, while fed conditions, proton-pump inhibitors, coating thickness and batch variability may also affect disintegration. The review therefore calls for sequential dissolution testing under gastric, small-intestinal and colonic conditions, stability data for intact capsules and, ideally, confirmation of release in humans. Measurements should extend beyond plasma because the relevant effects may arise from luminal action, mucosal exposure or systemic immune modulation. For a colon-targeted product, plasma concentration alone may underestimate mucosal exposure, while high systemic concentrations may be more relevant to toxicity.

Complete-formulation experiments offer more direct evidence than ingredient studies. In mouse models of chemically induced colitis, recognizable versions of the product have been associated with improvements in disease activity, colonic injury, inflammatory mediators, barrier proteins and microbial metabolites. More recent studies report a butyrate–GPR43–NCR-positive group 3 innate lymphoid cell axis, inhibition of NLRP3 inflammasome and STAT3-related signaling, changes in AGE-RAGE/NF-κB pathways, and ferroptosis-related endpoints. These findings connect microbial metabolism, epithelial integrity, inflammatory amplification and regulated cell death in biologically coherent ways. However, most experiments used small samples and acute disease models, administered treatment preventively or otherwise failed to reproduce clinical induction, and did not fully characterize the tested batches. Correlations between pathway markers and improved outcomes do not establish that each pathway is an independent target or causal mediator. Causal validation would require perturbations such as receptor antagonism, genetic manipulation, metabolite rescue or microbiota transfer.

Studies of individual ingredients broaden the biological plausibility while leaving the capsule’s effects unresolved. Matrine and oxymatrine have been associated in experimental systems with inflammatory signaling, oxidative stress, barrier protection and ferroptosis-related changes, and Sophora flavonoids have affected T-cell balance, epithelial pathways and microbial communities. Indigo naturalis, a processed source of indigoid compounds including indigo and indirubin, has shown short-term efficacy in a multicenter randomized trial involving people with active ulcerative colitis and may influence aryl hydrocarbon receptor pathways involved in mucosal defense. Sanguisorba extracts, Bletilla polysaccharides and licorice constituents have likewise produced supportive experimental findings. Yet these studies involve different doses, preparations, release profiles and safety conditions. Neither the presence of a compound in the capsule nor activity in a purified experimental system establishes that it reaches diseased tissue at a clinically relevant concentration or explains the complete product’s effect.

Clinical evidence comes mainly from older randomized studies. A multicenter single-blind trial reported efficacy for a composite Sophora colon-soluble capsule, and a later double-blind, double-dummy study involving 320 participants compared Fufangkushen colon-coated capsules with mesalazine over roughly eight weeks, finding broadly comparable short-term clinical and mucosal outcomes. Double-dummy masking is useful when dosage forms differ because it can help preserve participant and assessor blinding. However, a lack of a statistically significant difference does not prove equivalence unless an equivalence or noninferiority margin, adequate power, adherence, analysis population and confidence interval were specified in advance. The studies also had limited follow-up, older reporting standards and incomplete batch data. Meta-analyses reporting favorable “clinical effective rate” and traditional-pattern outcomes increase statistical precision but cannot remove small-study bias, selective publication, endpoint heterogeneity or uncertainty over whether different preparations were studied.

More recent clinical information remains provisional. A 2026 single-center cohort examined FSEC in combination with vedolizumab during induction and reported favorable week-14 clinical and endoscopic signals. Longer-term findings were sensitive to the analysis population, with a per-protocol signal not reproduced in the intention-to-treat analysis. Because treatment allocation was not randomized, baseline severity, clinician preference, affordability, prior response and adherence could have influenced the results; missing data could also have altered apparent durability. Such cohorts remain useful for feasibility, adherence, subgroup hypotheses and rare harms, but they cannot establish that FSEC adds benefit to biologic therapy. A prospective randomized add-on design would be needed to separate the capsule’s effect from concurrent treatment, regression to the mean and unequal follow-up.

Safety is particularly important because several ingredients carry recognizable hazards. Experimental matrine exposure has been linked to oxidative stress, mitochondrial apoptosis, disruption of Nrf2/GPX4 defenses, ferroptosis-related toxicity and altered cholesterol synthesis, although these findings cannot quantify clinical incidence in FSEC. Indigo naturalis has been associated with liver injury and pulmonary arterial hypertension, and ischemic colitis has also been reported during its use, a complication made difficult to recognize because worsening abdominal pain and bleeding can resemble an ulcerative colitis flare. Licorice metabolites can produce mineralocorticoid-like effects, including sodium retention, edema, hypertension, hypokalemia, metabolic alkalosis and arrhythmia. Risk may rise with prolonged use, older age, slow intestinal transit and exposure to other licorice products. Trials and pharmacovigilance should therefore document the exact product, batch, dose, duration, concomitant medicines and laboratory findings while actively monitoring liver chemistry, blood pressure, potassium, respiratory symptoms and cardiovascular events.

The review’s proposed next step is a linked chain from reproducible product to exposure, mechanism and clinical outcome. The first stage requires a reference dossier documenting botanical and processed-material identity, source, medicinal parts, preparation, excipients, quantitative multi-marker assays, chromatographic fingerprints, contaminants, stability and release performance. The same characterized batch should then be used for exposure studies, causal mechanism experiments and clinical assessment. A prospective multicenter randomized trial could evaluate clinical remission together with centrally read endoscopic improvement at week 8 or 12, with histology, fecal calprotectin, corticosteroid-free remission, quality of life, pharmacokinetics and safety as secondary outcomes. Maintenance follow-up would need to address relapse, hospitalization, colectomy and cumulative adverse events. Until such evidence is available, the review concludes that FSEC is a plausible and testable colon-targeted ethnopharmacological intervention, not a proven replacement for standard ulcerative colitis care.

Subject of Research: Evaluation of a five-material enteric-coated Chinese patent medicine for ulcerative colitis

Article Title: Five-flavor Sophora flavescens enteric-coated capsules for ulcerative colitis: ethnopharmacological rationale, pharmacology, clinical evidence, and safety

Article References: Ma, C., & Yang, C. (2026). Five-flavor Sophora flavescens enteric-coated capsules for ulcerative colitis: ethnopharmacological rationale, pharmacology, clinical evidence, and safety. Frontiers in Pharmacology, 17, 1972684. https://doi.org/10.3389/fphar.2026.1972684

Image Credits: AI Generated

DOI: 10.3389/fphar.2026.1972684

Keywords: ulcerative colitis, Sophora flavescens, Wuwei Kushen, Chinese patent medicine, ethnopharmacology, gut microbiome, colon-targeted delivery, clinical trials, drug safety, inflammatory signaling, Five-flavor, Sophora

The review covers research published from January 2020 through April 2026 that was identified through searches of PubMed, Scopus, Web of Science and Google Scholar. Eligible studies investigated network pharmacology for herbal or traditional-medicine therapies for RA and reported molecular targets, pathways, phytochemicals, docking, omics analyses or experimental validation. The review was critical in summarizing the evidence; it did not generate or analyse a new dataset.

Across the studies considered, network analyses repeatedly identified pathways involving TNF, NF-κB, IL-17, Toll-like receptor signaling, PI3K/Akt, MAPK, JAK/STAT, NLRP3, oxidative stress, angiogenesis and bone-related processes. These pathways are associated in the source studies with inflammatory signaling, immune-cell regulation, synoviocyte proliferation, apoptosis, osteoclastogenesis and joint destruction in RA.

Compounds that appeared repeatedly across different herbal preparations included quercetin, kaempferol, luteolin, berberine, celastrol and triptolide. The review describes computational and experimental associations between these compounds and targets such as TNF, IL-6, PTGS2, AKT1, RELA and MAPKs. For example, studies reported effects on inflammatory pathways, macrophage or fibroblast-like synoviocyte activity, and osteoclast-related processes in cell or animal models.

The evidence was not uniform. Some investigations included molecular docking, molecular or cellular assays, metabolomics or experiments in rheumatoid arthritis models. Others relied mainly on database-based target prediction, network construction and pathway enrichment. The review notes that comparisons among studies are difficult because proposed targets, herbal materials and experimental validation methods differ substantially.

Several findings were based on preclinical models rather than human clinical outcomes. Results reported in collagen-induced arthritis or other animal models, and in cultured synoviocytes or other cell systems, cannot by themselves establish safety or effectiveness in people with RA. A small number of reviewed studies included clinical trials, but the review emphasizes limited clinical validation overall.

The authors identify several limitations in the field. They report heterogeneity among public databases, including differences in compound-target annotations and update practices, which can introduce false positives and affect network results. They also note that static target-prediction methods may not represent dynamic cellular conditions and often do not establish whether a compound acts as an agonist, antagonist or other modulator. Pharmacokinetics, botanical variation, extraction methods and formulation standardization remain additional issues.

Overall, the review concludes that network pharmacology offers a framework for target prioritization and mechanism-based investigation of multi-component herbal medicines in RA. It presents the approach as a possible bridge between traditional medicinal knowledge and systems-based drug discovery, while emphasizing that computational predictions need standardized products, experimental confirmation and controlled clinical studies before they can support therapeutic claims.

Subject of Research: Network pharmacology analysis of herbal medicines and bioactive compounds in rheumatoid arthritis

Article Title: Molecular mechanisms of herbal medicines and bioactive compounds in rheumatoid arthritis: a comprehensive network pharmacology perspective

Article References: Jasna, T. J., Sandra, K. S., Vithalkar, M. P., Vijaykumar, D., & Nayak, Y. (2026). Molecular mechanisms of herbal medicines and bioactive compounds in rheumatoid arthritis: a comprehensive network pharmacology perspective. Molecular Biology Reports, 53(1), Article 1559. https://doi.org/10.1007/s11033-026-12727-5

Image Credits: AI Generated

DOI: 10.1007/s11033-026-12727-5

Keywords: Rheumatoid arthritis, Network pharmacology, Herbal medicine, Phytochemicals, Inflammatory signaling, Systems biology, Molecular docking, Drug discovery, Molecular, mechanisms, herbal, medicines

The rationale for the study stems from a fundamental problem in clinical medicine: syndromes defined by symptoms rather than objective biomarkers are notoriously difficult to separate from one another. Fibromyalgia, one of the most common rheumatic disorders, shares features such as chronic widespread pain, fatigue, and cognitive difficulties with a range of other conditions, including rheumatoid arthritis. That overlap complicates diagnostic evaluation, because a patient with early or atypical rheumatoid arthritis may present much like someone with fibromyalgia, and vice versa. The researchers therefore designed their experiment to ask a deliberately narrow question: could an integrated spectroscopic and metabolomic workflow distinguish fibromyalgia from rheumatoid arthritis at the molecular level, using small blood samples and analytical methods fast enough to imagine a future clinical assay?

The study enrolled 70 participants: 40 with fibromyalgia, 20 with rheumatoid arthritis, and 10 healthy controls. The team was acutely aware that the weakest link in any metabolomics experiment is often not the instrument but the sample handling that precedes it. Preanalytical variables, such as how blood is collected, stored, and extracted, can swamp genuine biological signals with artifacts. To address this, the researchers systematically examined sources of preanalytical interference and compared multiple extraction solvents, ultimately finding that methanol alone and a methanol and 1-butanol mixture provided the broadest coverage of the metabolome. This methodological rigor matters because it establishes a reproducible foundation on which larger validation studies can be built, rather than a one-off result that collapses when protocols change.

Fourier-transform infrared spectroscopy, the first pillar of the workflow, is a technique more familiar to food scientists and chemists than to rheumatologists. It works by shining infrared light through a sample and measuring which wavelengths are absorbed. Different chemical bonds, such as those in proteins, lipids, carbohydrates, and nucleic acids, absorb characteristic frequencies of infrared radiation, so the resulting spectrum acts as a composite portrait of the sample’s entire molecular composition. Crucially, FTIR requires minimal sample preparation, produces results in minutes, and can be miniaturized into relatively inexpensive benchtop instruments. The trade-off is that an FTIR spectrum is a dense, overlapping pattern of absorptions rather than a clean list of identified compounds, which is why the researchers paired it with mass spectrometry to assign chemical meaning to the spectral differences they observed.

Mass spectrometry-based metabolomics, the second pillar, takes the opposite approach. By ionizing small molecules extracted from blood and measuring their mass-to-charge ratios, the technique can identify and quantify individual metabolites, the thousands of small molecules produced by metabolism. Where FTIR offers speed and simplicity, mass spectrometry offers specificity and chemical annotation. The idea behind the integrated workflow is elegant: use mass spectrometry to discover which metabolites differ between patient groups, then test whether the fast FTIR measurement can capture the same information, effectively using the slower, richer technique as a ground truth for calibrating a rapid screening method.

To turn raw spectral and metabolomic data into diagnostic insight, the team applied machine learning methods drawn from the chemometrics tradition, particularly partial least squares discriminant analysis for classification and partial least squares regression for modeling continuous relationships. These multivariate techniques are well suited to spectroscopic data, where thousands of correlated variables must be compressed into a few latent factors that capture the most biologically meaningful variation. Importantly, the researchers adjusted their models for covariates and used internal cross-validation to estimate performance, guarding against the overfitting that has undermined many small biomarker studies. When they compared fibromyalgia against rheumatoid arthritis, the covariate-adjusted, cross-validated model achieved an area under the receiver operating characteristic curve of 0.84, a figure indicating useful, though not yet definitive, discriminatory power.

Beyond classification, the metabolomic analysis revealed which specific molecules were driving the separation between groups. The tentatively annotated contributors included oligopeptides, short chains of amino acids; inosine monophosphate, a nucleotide involved in purine metabolism; and several signaling lipid molecules, including members of the N-acylethanolamine and monoacylglycerol families, which are known to participate in pain and inflammatory signaling. The researchers suggest that these findings may be associated with dysregulation of oxidative-stress and inflammatory-signaling pathways, a picture broadly consistent with earlier hypotheses that fibromyalgia involves low-grade neuroimmune perturbation rather than a purely psychological origin. The team was careful to describe these annotations as tentative, reflecting the exploratory nature of the study and the inherent caution required when assigning chemical identities in untargeted metabolomics.

Perhaps the most technically significant result came from the regression analysis linking the two platforms. The partial least squares regression models showed strong correlations between FTIR spectral features and the relative mass spectrometry intensities of several metabolites, including inosine monophosphate, N-acylethanolamines, monoacylglycerols, fructosyl phenylalanine, fructosyl isoleucine, the dipeptide Ser-Phe, and 3,4,5-trihydroxypentanoylcarnitine, with coefficients of determination of at least 0.70. In practical terms, this means the infrared spectrum, which can be acquired in minutes with minimal preparation, carries enough information to predict the abundance of specific biologically interesting metabolites measured by far slower and costlier mass spectrometry. This is precisely the kind of cross-platform correspondence that would be needed to develop a rapid FTIR-based screening assay for clinical use.

The authors and outside observers alike will emphasize that this is a proof of concept, not a diagnostic test. The sample sizes were modest, the healthy control group especially small, and the classification performance was assessed with internal cross-validation rather than on an independent external cohort. Metabolite annotations remain tentative pending confirmation with authentic standards, and the study did not address whether the molecular signatures are specific to fibromyalgia or might overlap with other pain syndromes. The researchers themselves frame the work as a foundation for larger, independent clinical validation studies that will need to determine the reproducibility and diagnostic performance of the molecular signatures across diverse populations and clinical sites.

Even with those caveats, the study represents a meaningful step toward an objective molecular characterization of a condition that has often been dismissed or misunderstood. The workflow demonstrates that preanalytical variables can be controlled, that spectroscopy and metabolomics can be integrated in a coherent analytical pipeline, and that fibromyalgia and rheumatoid arthritis, two conditions that clinicians frequently struggle to distinguish, leave distinguishable chemical traces in blood. If subsequent validation studies confirm these findings in larger cohorts, the long-term vision is a rapid, inexpensive infrared screening assay that could shorten the diagnostic odyssey for millions of patients. The research was funded by the National Institutes of Health through NINDS grant R61/R33 NS117211 and GR122808, and the study was approved by the Institutional Review Board of the University of Texas at Austin, with written informed consent obtained from all participants.

Subject of Research: Integrating FTIR spectroscopy and mass spectrometry metabolomics for molecular profiling and diagnosis of fibromyalgia

Article Title: Toward rapid molecular profiling of fibromyalgia: an exploratory study integrating vibrational spectroscopy and metabolomics

Article References: Nuguri, S. M., Rodriguez-Saona, L., Gao, C., Bao, H., Sebastian, K. R., Osuna-Diaz, M. M., Giusti, M. M., Yu, L., Lamo Castellvi, S. D., & Hackshaw, K. V. (2026). Toward rapid molecular profiling of fibromyalgia: an exploratory study integrating vibrational spectroscopy and metabolomics. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-08919-z

Image Credits: AI Generated

DOI: 10.1186/s12967-026-08919-z

Keywords: fibromyalgia, metabolomics, FTIR spectroscopy, mass spectrometry, biomarkers, rheumatoid arthritis, molecular profiling, machine learning, PLS-DA, oxidative stress, inflammatory signaling, diagnostics

GPR84 belongs to a subgroup of GPCRs that respond to medium-chain fatty acids, the metabolic fragments released when fats are broken down. Because these fragments accumulate in tissues under metabolic stress, GPR84 is thought to act as a metabolic sensor for the immune system, translating changing lipid levels into altered cellular behavior. Decades of pharmacological studies have linked the receptor to macrophages, neutrophils and other innate immune cells, where its activation has been associated with amplified production of inflammatory signaling molecules. That association made GPR84 an attractive drug target for companies pursuing anti-inflammatory therapies, and it also made the receptor a cautionary tale: several clinical candidates targeting it were halted, in some cases because the biology proved more complicated than early animal studies suggested.

The central problem has been that GPCRs are not simple on-off switches. They are dynamic molecular machines that sample a range of conformations, and different ligands can stabilize different subsets of those conformations. A ligand that locks the receptor into a fully active shape will recruit signaling proteins robustly, while a ligand that favors inactive shapes will silence the pathway. But many ligands do something subtler: they stabilize partially active conformations, or they favor active shapes in one signaling branch while leaving others untouched. Without structural information, medicinal chemists were essentially adjusting molecular shapes blindly, hoping that small changes in a ligand scaffold would produce predictable changes in receptor behavior.

The new study addresses that gap by capturing GPR84 in two distinct functional states, allowing the researchers to compare the receptor’s architecture when it is being activated against its architecture when it is being blocked or modulated. Structures determined in multiple states are technically demanding, because a membrane-embedded receptor must be stabilized in each conformation long enough to be imaged at atomic resolution. Achieving this typically requires engineered variants, stabilizing antibodies or nanobodies, and carefully chosen ligands that preferentially hold the receptor in the desired state. The resulting paired structures function like two frames of a molecular movie, revealing which helices shift, which side chains rotate, and which structural water molecules rearrange as the receptor transitions between resting and signaling-competent forms.

Comparing the two states highlights the allosteric heart of the receptor. In GPCRs, ligand binding at a pocket nestled among the transmembrane helices is transmitted through a conserved relay of hydrogen bonds, salt bridges and hydrophobic contacts to the intracellular face, where G proteins and other effectors dock. The dual-state GPR84 structures delineate how agonist binding contracts this relay into the canonical active arrangement, with an inward movement of the extracellular portion of a key transmembrane helix and a corresponding outward swing on the intracellular side that opens the effector-binding cavity. In the inactive or antagonist-bound state, that same helix relaxes outward, the intracellular cavity collapses, and the network of polar interactions reconfigures into a pattern incompatible with effector coupling. The residue-by-residue map of these changes gives chemists concrete positions to target when they want to bias the equilibrium toward one state or the other.

Crucially, the structural work is not left to stand alone. The authors couple it with functional assays performed in immune cells, measuring how well each ligand drives or suppresses downstream signaling and, importantly, how it affects inflammatory outputs such as cytokine release. This combination is what elevates the study from structural description to pharmacological instruction. A structure can suggest that a compound should be an agonist, but only cellular assays reveal the potency, the efficacy ceiling, and whether the compound behaves as a full agonist, a partial agonist or a biased ligand in a physiologically relevant context. By testing ligands across the spectrum, the researchers could correlate specific structural features of the binding pocket with specific functional consequences, effectively building a translation table between atomic geometry and immune cell behavior.

One of the more interesting implications concerns ligand bias, the phenomenon in which a receptor signals preferentially through one intracellular pathway over another. For GPR84, whose activation intersects with inflammatory programs in macrophages, a biased ligand could in principle dampen harmful signaling while preserving useful functions, or vice versa. The dual-state structures provide a mechanistic handle on bias: ligands that engage only part of the activation relay, or that fail to complete certain helical movements, may recruit one effector but not another. The immune functional assays then quantify what that partial engagement means for cytokine production, giving drug developers a rational framework for designing compounds with tailored signaling profiles rather than accepting whatever profile a scaffold happens to produce.

The study also speaks to the thorny issue of species differences, which has plagued GPR84 drug development. Synthetic agonists developed against the human receptor have often shown sharply different potency in mouse models, complicating the interpretation of preclinical efficacy studies and contributing to the sector’s clinical disappointments. Although the structures presented are of the human receptor, the detailed pocket architecture allows researchers to pinpoint which residues differ across species and to predict, before expensive animal work, whether a given compound is likely to translate. That kind of structural triage could save years of effort and redirect resources toward candidate molecules with a realistic chance of reproducing human biology in animal systems.

Beyond immediate drug design, the work contributes to a broader shift in GPCR pharmacology toward state-based thinking. Rather than classifying ligands simply as agonists, antagonists or inverse agonists, the field increasingly describes them by the conformational ensembles they stabilize and the signaling outputs those ensembles produce. GPR84, with its metabolic ligands, its immune cell expression and its checkered clinical history, is an ideal test case for this framework. The demonstration that paired structures plus immune assays can jointly explain and predict pharmacological behavior provides a template that other lipid-sensing and metabolite-sensing receptors could follow, particularly those where immune modulation is the therapeutic goal.

For patients, the significance lies in what this molecular clarity could eventually enable. Chronic inflammatory and metabolic diseases, including conditions involving macrophage-driven tissue damage, remain areas of substantial unmet need, and receptors that sense the metabolic environment of inflamed tissue are logical points of intervention. By showing exactly how ligands of different pharmacological classes occupy the GPR84 binding pocket and drive or block its conformational changes, the study turns a previously opaque target into an addressable one. The next steps, testing structure-guided ligand designs and validating their immune effects in disease models, will determine how quickly this structural knowledge moves from the pages of a journal toward the clinic, but the roadmap for modulating GPR84 rationally is now drawn.

Subject of Research: Structural and pharmacological modulation of the lipid-sensing immune receptor GPR84

Article Title: Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays

Article References: Choi, M. K., Park, D. J., Kim, P., Choi, H. S., Myung, S., Yoo, Y., Chang, N., Yoon, G.-Y., Kang, H. J., Ha, S.-J., & Cho, H.-S. (2026). Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays. Experimental & Molecular Medicine. https://doi.org/10.1038/s12276-026-01841-w

Image Credits: AI Generated

DOI: 10.1038/s12276-026-01841-w

Keywords: GPR84, G protein-coupled receptor, dual-state structures, immune functional assays, ligand bias, inflammatory signaling, macrophages, medium-chain fatty acids, structural biology, drug discovery, Pharmacological, modulation