GRI Bio Presents New Phase 2a Data at ERS 2026 Defining GRI-0621's Mechanism of Action in IPF Across Nine Mechanistic Pillars

Phase 2a IPF study links GRI-0621’s multi-modal repair biomarkers with exploratory FVC benefits and a favorable 12-week safety profile.

Rhea-AI Summary

GRI Bio (GRI) reported new Phase 2a IPF data for oral RARβ/γ agonist GRI-0621, showing exploratory lung function and mechanistic signals after 12 weeks.

In 35 randomized patients, 39% on GRI-0621 achieved ≥30 mL FVC increase versus 20% on placebo, rising to 50% with background antifibrotics. Only 8% on GRI-0621 had ≥10% FVC decline versus 20% on placebo, and placebo-adjusted mean FVC change was +99 mL overall and +139 mL on standard-of-care therapy. Ten post hoc FVC sensitivity analyses remained directionally positive. Biomarker data across RNA sequencing, serum ECM markers and spectral flow cytometry supported nine pre-specified mechanistic pillars, including immune re-balancing, myofibroblast inhibition, fibrolysis and basement-membrane repair. GRI-0621 was well tolerated with 0% serious treatment-emergent adverse events versus 8% on placebo and lower rates of cough, dyspnea and diarrhea.

Positive

• FVC improvement: 39% on GRI-0621 vs 20% on placebo achieved ≥30 mL increase at Week 12, rising to 50% with background antifibrotics
• Reduced FVC decline: ≥10% FVC drop in 8% on GRI-0621 vs 20% on placebo, a 60% relative reduction
• Placebo-adjusted FVC: +99 mL overall and +139 mL on background standard-of-care antifibrotic therapy at Week 12
• Robustness analyses: ten post hoc FVC sensitivity analyses stayed directionally positive, converging on +40–65 mL overall and +67–89 mL on background SOC
• Mechanistic validation: nine mechanistic pillars supported by concordant signals from at least two of four biomarker modalities
• Safety profile: 0% serious treatment-emergent adverse events on GRI-0621 vs 8% on placebo, with less cough (0% vs 25%), dyspnea (4% vs 17%) and diarrhea (17% vs 33%)

Negative

• Small, short study: 35 patients treated for 12 weeks limits statistical power and long-term assessment
• Exploratory endpoint: FVC was exploratory and the trial was not powered for statistical significance despite positive trends

News Explained

GRI Bio presented results from its 12-week Phase 2a study and says they support advancing GRI-0621 to evaluation in a 52-week study; the release describes that as a future program step, not a study already reported as begun.

Market Context

+8.48% followed the Aug 24 announcement that Phase 2a data would be presented; this release reported...

Analysis

+8.48% followed the Aug 24 announcement that Phase 2a data would be presented; this release reported those results and described evaluation in a 52-week study. An effective S-3 filed Jan 29 covers up to $250,000,000.

Key Figures

Study size: 35 patients FVC responders: 39% vs. 20% placebo; 50% with background SOC Placebo-adjusted FVC: +99 mL overall; +139 mL with background SOC +4 more

Study size

35 patients

Phase 2a IPF study

FVC responders

39% vs. 20% placebo; 50% with background SOC

Patients with FVC increase of ≥30 mL at Week 12

Placebo-adjusted FVC

+99 mL overall; +139 mL with background SOC

Change from baseline at Week 12

FVC decline reduction

60%

Relative reduction in accelerated-decline event rate

Serious adverse events

0% vs. 8% placebo

Treatment-emergent serious adverse events over 12 weeks

Treatment-emergent cough

0% vs. 25% placebo

Safety comparison over 12 weeks

Statistically significant biomarkers

18 of 72 at FDR<0.05; 13 readouts at p<0.05

RNA sequencing and spectral flow cytometry

Historical Context

2 past events · Latest: Aug 24

2 events

1. Aug 24

   Phase 2a data notice

   24h Move

   +8.5%

   Company announced planned ERS presentations covering Phase 2a lung function, biomarkers and safety

2. May 14

   Q1 results and data

   24h Move

   -4.9%

   Company reported Phase 2a safety results and exploratory FVC improvements for GRI-0621

24h Move is the share-price change in the day after each event; other market factors may also have contributed.

Key Terms

fvc, ipf, bronchoalveolar lavage, pharmacodynamic, +2 more

6 terms

fvc medical

"placebo-adjusted FVC change from baseline at Week 12"

Forced vital capacity (FVC) is a lung function measurement that records how much air a person can forcefully exhale after taking the deepest breath possible, similar to timing and measuring a strong, single blow to extinguish a candle. Investors care because FVC is a common clinical trial endpoint for respiratory drugs and devices; meaningful improvements or declines can influence trial success, regulatory approval odds, labeling, and ultimately commercial prospects.

ipf medical

"patients with idiopathic pulmonary fibrosis ("IPF")"

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease where scar tissue builds up in the lungs for reasons doctors don't fully understand, making it harder to breathe over time. For investors, IPF matters because it represents a clear medical need and a regulated market for treatments, so progress in clinical trials, regulatory approvals, or new therapies can materially affect the value of companies working on drugs or devices for this condition—much like a new road that could open access to a previously hard-to-reach town.

bronchoalveolar lavage medical

"paired blood and bronchoalveolar lavage samples"

A bronchoalveolar lavage is a medical procedure that rinses a small area of the lung with fluid and then collects that fluid for analysis, like flushing and examining the inside of a pipe to see what’s inside. Investors care because results can reveal infection, inflammation, or drug-related lung effects that influence clinical trial outcomes, regulatory decisions and market perception of respiratory therapies or safety profile of systemic drugs.

pharmacodynamic medical

"confirming pharmacodynamic engagement of the retinoic acid receptor pathway"

Pharmacodynamic describes how a drug acts on the body — the biological effects it produces, how strong those effects are, and how long they last. For investors, pharmacodynamic data show whether a treatment actually works and at what dose, shaping expectations about a drug’s safety, effectiveness, regulatory success and market potential; think of it like testing how well a key turns a lock and whether it reliably opens the door.

fdr technical

"Eighteen anchor transcripts reached statistical significance (FDR<0.05)"

False discovery rate (FDR) is the proportion of reported positive findings that are actually false when many tests or comparisons are made. Think of checking dozens of lottery tickets: even if a few look like winners by chance, FDR estimates how many of those apparent wins are likely errors. For investors, FDR matters because it helps judge whether promising study results, subgroup analyses, or screening signals are likely real or just statistical flukes that could mislead valuations and expectations.

rarβ/γ-selective agonist medical

"the Company's oral retinoic acid receptor ("RAR") β/γ-selective agonist"

A rarβ/γ-selective agonist is a drug or compound that binds to and activates the beta and gamma subtypes of retinoic acid receptors (RARβ and RARγ), which are cellular proteins that regulate genes involved in cell growth, differentiation, and inflammation. Because it targets only those receptor subtypes rather than all RARs, it aims to produce specific therapeutic effects while reducing actions tied to other receptor types; for investors, selectivity can mean a clearer development path, distinct clinical uses, and a different safety or side-effect profile compared with nonselective retinoid drugs.

AI-generated analysis. How Rhea-AI works. Not financial advice.

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New whole blood RNA sequencing data identified coordinated, consistent change in genes governing immune re-balancing, myofibroblast inhibition, fibrolysis, basement membrane repair, re-epithelialization, antitussive effect and GI protection

Signals observed from at least two independent measurement modalities, including RNA sequencing, serum extracellular matrix biomarkers, spectral flow cytometry and clinical readouts, supported each of the nine pre-specified mechanistic pillars, defining a repair phenotype with anti-fibrotic and pro resolving effects

Approximately 2x–2.5x as many GRI-0621-treated patients experienced an FVC increase compared with placebo; placebo-adjusted FVC change from baseline at Week 12 was +99 mL overall and +139 mL on background standard-of-care antifibrotic therapy

Totality of Phase 2a findings supports advancement of GRI-0621 in the IPF program and further evaluation in a longer-duration study

LA JOLLA, CA, Sept. 08, 2026 (GLOBE NEWSWIRE) -- GRI Bio, Inc. (NASDAQ: GRI) ("GRI Bio" or the "Company"), a biotechnology company developing innovative therapies for inflammatory, fibrotic and autoimmune diseases, today announced new translational biomarker data from the Phase 2a GRI-0621-IPF-02 study evaluating GRI-0621 (oral tazarotene) in patients with idiopathic pulmonary fibrosis ("IPF"). The new data, together with the study's lung function and safety results, were presented in a late-breaking oral presentation and three posters at the 2026 European Respiratory Society ("ERS") Congress in Barcelona, Spain.

The data presented at ERS integrate, for the first time, four independent measurement modalities from the same 35-patient study population: whole-blood RNA sequencing, an expanded 12-marker serum extracellular matrix ("ECM") neo-epitope panel, 28-color spectral flow cytometry of paired blood and bronchoalveolar lavage samples, and clinical and patient-reported readouts. Across these modalities, the Phase 2a evidence resolves into nine coherent mechanistic pillars that define how selective RARβ/γ agonism by GRI-0621 acts in IPF: immune re-balancing, reduced lung injury, myofibroblast inhibition, fibrolysis, basement-membrane repair, re-epithelialization, FVC stabilization, antitussive effect and gastrointestinal protection. Each pillar is supported by direction-consistent signals from at least two independent modalities.

Newly reported observations from whole-blood RNA sequencing of 72 curated anchor genes, 28-color spectral flow cytometry of paired blood and bronchoalveolar lavage samples and an expanded 12-marker serum ECM panel provide concordant, direction-consistent signals across the mechanistic pillars. Eighteen anchor transcripts reached statistical significance (FDR<0.05), including ALDH1A2 ↑ confirming pharmacodynamic engagement of the retinoic acid receptor pathway, and 13 flow cytometry readouts reached p<0.05. Key concordant signals included:

• Dismantling of the pro-fibrotic Th2 response: A Th2-to-Th1 shift was observed at both the RNA and protein levels: CCR4 ↓, IL4 ↓ and IL13 ↓ by RNA sequencing, mirrored by flow cytometry showing CCR4 ↓ across six immune lineages, IL-4 ↓, IL-13 ↓ and IFN-γ ↑, together with Th17 inhibition (IL-17A ↓), reduced TGF-β and restored iNKT T-cell receptor expression consistent with iNKT inactivation increased HLA-DR on lung macrophages indicates immune re-programming rather than immune suppression.
• Myofibroblast inhibition through suppression of the TGF-β and ROCK2 pathways: RNA sequencing suggested coordinated downregulation along the TGF-β axis (ADAMTS1 ↓, F2R ↓, TXNDC5 ↓, LTBP1 ↓ and TGFBR2 ↓, with upregulation of the negative-feedback regulators SMAD6/7 ↑ and PMEPA1 ↑, and downstream FN1 ↓, CCN2/CTGF ↓ and TGFB1 ↓) and the ROCK2 contractility axis (RHOA/B ↓ → ROCK2 ↓ and MYL12A ↓ → ACTA2 ↓, LIMK1 ↓, CFL1 ↓, TLN1/VCL ↓ and MRTFA ↓ → SRF ↓), corroborated by reduced TGF-β protein on flow cytometry and reduced serum synthesis of the fibrillar collagens (PRO-C3 ↓, PRO-C6 ↓).
• Fibrolysis: Serum degradation markers of type III and type VI collagen (C3M ↑, CTX-III ↑, C6M ↑) rose while their synthesis markers (PRO-C3 ↓, PRO-C6 ↓) fell, shifting all three synthesis-to-degradation ratios toward net fibrolysis (placebo-adjusted PRO-C3/C3M −13.6, PRO-C3/CTX-III −15.9 and PRO-C6/C6M −14.0 percentage points), concordant with RNA sequencing (ADAMTS1 ↓, MMP1 ↓, PLOD1 ↓, COL1A2 ↓, COL3A1 ↓, COL6A2/A3 ↓).
• Basement-membrane repair: Type IV collagen, the network-forming collagen of the alveolar basement membrane, moved in the opposite direction to the fibrillar collagens. Serum PRO-C4 ↑ (synthesis) and C4Ma3 ↓ (degradation), a placebo-adjusted PRO-C4/C4Ma3 shift of +13.6 percentage points toward net repair, concordant with RNA sequencing upregulation of the basement-membrane genes COL4A1/A2 ↑, LAMA3 ↑ and COL17A1 ↑ and the anti-fibrotic matricellular protein CCN3 ↑.
• AT2/AT1 re-epithelialization: Downstream of basement-membrane repair, RNA sequencing suggested a coordinated alveolar repair program: ALDH1A2 ↑, NAPSA ↑ and SFTPB ↑ (type 2 alveolar epithelial cell identity), NUPR1 ↑, CRB3 ↑, CAV1 ↑ and DLK1 ↑ (AT2-to-AT1 differentiation and restored epithelial polarity), and AGER ↑ and AQP5 ↑ (type 1 alveolar epithelial cell markers), with FVC and dyspnea as functional readouts.
• Antitussive: Treatment-emergent cough was 0% on GRI-0621 versus 25% on placebo, consistent with RNA sequencing evidence of epithelial-barrier restoration (CAV1 ↑, TNFSF10/TRAIL ↓), reduced C-fiber excitability (HTR1B ↓, TAC3 ↓, CALCB ↓) and reduced peripheral sensory transduction (TRPA1 ↓, TRPV1 ↓).
• GI protection: Diarrhea (17% vs. 33%) and weight loss (0% vs. 17%) were less frequent on GRI-0621 than placebo despite higher background nintedanib use in the GRI-0621 arm, consistent with RNA sequencing showing reduced mucosal inflammatory tone and iNKT inhibition (ARG2 ↓, CCR4 ↓, MRC1 ↓) and upregulation of mucosal-repair and vascular-protective growth factors (FGF2 ↑, FGFR1/3 ↑, FLT1 ↑, FLT4 ↑, PDGFA/B/C ↑, VEGFA ↑).
  
  

"What is emerging from the Phase 2a dataset is a profile we believe is unique among IPF programs," said Marc Hertz, PhD, Chief Executive Officer of GRI Bio. "Approved antifibrotics slow lung function decline but have not been shown to rebuild lung architecture. With GRI-0621, we observed an anti-fibrotic effect, inhibition of myofibroblasts and a shift toward net breakdown of fibrillar collagen, but we also saw something more: a concordant signal of basement-membrane repair, with a net gain in type IV collagen at both the gene and protein level, followed by activation of the genes that drive type 2 alveolar cells to become the type 1 cells that line a functioning alveolus. Anti-fibrotic activity, basement-membrane repair and re-epithelialization, observed together and in the same patients across four independent modalities, is the signature of a repair phenotype. We believe this is why we see the FVC signal we do after only 12 weeks, and it is what gives us confidence to advance GRI-0621 into a longer-duration study."

The exploratory lung function findings were consistent with the mechanistic data. At Week 12, 39% of GRI-0621-treated patients experienced an FVC increase of ≥30 mL compared with 20% on placebo, rising to 50% among patients receiving background standard-of-care ("SOC") antifibrotic therapy, approximately 2x–2.5x the placebo responder rate. At the other end of the distribution, only 8% of GRI-0621-treated patients experienced an FVC decline of ≥10% compared with 20% on placebo, a 60% relative reduction in the accelerated-decline event rate. Placebo-adjusted FVC change from baseline at Week 12 was +99 mL overall and +139 mL on background SOC. Because spirometry is subject to visit-to-visit variability and outliers in a small study, a family of ten post hoc robustness sensitivity analyses were performed. Every analysis remained directionally positive, with estimates converging on +40 to +65 mL overall and +67 to +89 mL in the background SOC subset. FVC was an exploratory endpoint and the study was not powered for statistical significance.

GRI-0621 was well tolerated over 12 weeks. There were no serious treatment-emergent adverse events in the GRI-0621 arm (0% vs. 8% on placebo) and no drug-related serious adverse events. Adverse events were consistent with the known retinoid class profile (dry lips, dry skin, arthralgia and myalgia), all Grade 1–2 and managed with routine supportive care. GRI-0621-treated patients reported less treatment-emergent cough (0% vs. 25%), dyspnea (4% vs. 17%) and diarrhea (17% vs. 33%) than placebo, despite higher background nintedanib use in the GRI-0621 arm. No clinically meaningful changes in liver enzymes, triglycerides or LDL cholesterol were observed and no night vision, hearing or neuropsychiatric events were reported.

Key Findings from the Phase 2a GRI-0621-IPF-02 Study

• Nine mechanistic pillars defined: Direction-consistent signals from at least two of four independent measurement modalities supported each of the nine pre-specified mechanistic pillars: immune re-balancing, reduced lung injury, myofibroblast inhibition, fibrolysis, basement-membrane repair, re-epithelialization, FVC stabilization, antitussive effect and GI protection.
• Strong concordance across biomarker modalities: RNA sequencing (18 of 72 anchor transcripts at FDR<0.05), spectral flow cytometry (13 readouts at p<0.05) and serum ECM biomarkers were direction-consistent in the same patients, showing dismantling of the Th2 response, suppression of the TGF-β and ROCK2 pathways, net fibrolysis of type III and VI collagen, net repair of type IV collagen basement membrane and an AT2-to-AT1 re-epithelialization program, alongside antitussive and GI-protective signals.
• Favorable FVC responder and decline rates: 39% of GRI-0621-treated patients experienced an FVC increase of ≥30 mL compared with 20% on placebo, increasing to 50% among patients receiving background SOC therapy. Only 8% of GRI-0621-treated patients experienced an FVC decline of ≥10% compared with 20% on placebo, a 60% relative reduction.
• Positive effect on FVC: Placebo-adjusted FVC change from baseline at Week 12 was +99 mL overall and +139 mL among patients receiving background SOC antifibrotic therapy.
• Robust FVC sensitivity analyses: All ten post hoc robustness sensitivity analyses of the FVC endpoint remained directionally positive, with estimates converging on +40 to +65 mL overall and +67 to +89 mL on background SOC. FVC was an exploratory endpoint and the study was not powered for statistical significance.
• Favorable tolerability: GRI-0621 was well tolerated over 12 weeks, with no serious treatment-emergent adverse events compared with 8% on placebo, zero drug-related serious adverse events, less cough (0% vs. 25%), dyspnea (4% vs. 17%) and diarrhea (17% vs. 33%) than placebo and no hepatic, lipid, visual, auditory or neuropsychiatric safety signals.
  
  

Presentation and Posters

• Late-Breaking Oral
  

Safety, translational biomarkers and lung function with the oral RARβ/γ-selective agonist GRI-0621 in idiopathic pulmonary fibrosis: a Phase 2a randomised, double-blind, placebo controlled trial (GRI-0621-IPF-02)

• Translational Biomarkers
  

GRI-0621 Phase 2a biomarker study in patients with IPF using gene expression, immune cell activity and collagen markers supports a repair phenotype with strong anti-fibrotic and pro-resolving effects

• Lung Function
  

GRI-0621 phase 2a biomarker study in patients with IPF: GRI-0621 has a positive effect on FVC after 12 weeks of treatment

• Safety
  

GRI-0621 phase 2a biomarker study in patients with IPF: a safety signal demonstrating favorable tolerability

GRI-0621-IPF-02 (NCT06331624) was a randomized, double-blind, placebo-controlled Phase 2a study evaluating the safety, translational biomarkers and exploratory lung function of GRI-0621, the Company's oral retinoic acid receptor ("RAR") β/γ-selective agonist. Thirty-five patients with IPF were randomized 2:1 to receive GRI-0621 4.5 mg once daily (n=23) or placebo (n=12) for 12 weeks, with 80% receiving background pirfenidone or nintedanib. Safety was the pre-specified primary endpoint.

Taken together, the Phase 2a data define a mechanism of action for GRI-0621 in IPF that couples immune re-balancing to matrix catabolism and alveolar epithelial repair, supported by direction-consistent signals across four independent modalities, together with a positive effect on FVC after 12 weeks of treatment and favorable tolerability. The Company believes the findings support advancement of GRI-0621 in the IPF program and evaluation in a 52-week study, including concomitant with background pirfenidone or nintedanib.

About GRI Bio, Inc.

GRI Bio is a clinical-stage biopharmaceutical company focused on developing innovative therapies for inflammatory, fibrotic and autoimmune diseases. The Company's lead program, GRI-0621, is an oral RARβ/γ-selective agonist being developed for the treatment of idiopathic pulmonary fibrosis (IPF), a progressive and life-threatening fibrotic lung disease with significant unmet need. GRI-0621 is designed to modulate pathways associated with inflammation, fibrosis and tissue repair and is being evaluated as a potential novel oral therapeutic for patients with IPF.

In addition to GRI-0621, the Company is also developing a pipeline of novel type 2 diverse NKT ("dNKT") agonists for the treatment of systemic lupus erythematosus. Additionally, with a library of over 500 proprietary compounds, GRI Bio has the ability to fuel a growing pipeline.

Forward-Looking Statements

This press release contains "forward-looking statements" within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements may be identified by the use of words such as "anticipate," "believe," "contemplate," "could," "estimate," "expect," "intend," "seek," "may," "might," "plan," "potential," "predict," "project," "target," "aim," "should," "will," "would," or the negative of these words or other similar expressions. These forward-looking statements are based on the Company's current beliefs and expectations. Forward-looking statements include, but are not limited to, statements regarding: the Company's expectations with respect to development and commercialization of the Company's product candidates, the timing of initiation or completion of clinical trials and availability of resulting data, the potential benefits and impact of the Company's clinical trials and product candidates and any implication that the data or results observed in preclinical trials or earlier studies, topline or interim data or trials will be indicative of results of later studies or clinical trials or final data, the Company's beliefs and expectations regarding potential shareholder value and future financial performance, the Company's beliefs about the timing and outcome of regulatory approvals and potential regulatory approval pathways, the Company's expected future milestones, shareholder value and the length of time the Company's current resources will fund its planned operations (which current estimate assumes only initial preparatory activities for GRI-0621 as substantial additional capital or resources will be required to fund a Phase 2b clinical trial of GRI-0621). Actual results may differ from the forward-looking statements expressed by the Company in this press release and consequently, you should not rely on these forward-looking statements as predictions of future events. These forward-looking statements are subject to inherent uncertainties, risks and assumptions that are difficult to predict, including, without limitation risks related to: (1) the Company's inability to maintain the listing of the Company's common stock on The Nasdaq Capital Market and to comply with applicable listing requirements; (2) changes in applicable laws or regulations; (3) the inability of the Company to raise financing in the future; (4) the success, cost and timing of the Company's product development activities; (5) the inability of the Company to obtain and maintain regulatory clearance or approval for its respective products, and any related restrictions and limitations of any cleared or approved product; (6) the inability of the Company to identify, in-license or acquire additional technology; (7) the inability of the Company to compete with other companies currently marketing or engaged in the development of products and services that the Company is currently developing; (8) the accuracy of the estimated size and growth potential of the markets for the Company's products and services, and its ability to serve those markets, either alone or in partnership with others; (9) that later data or clinical trials may be inconsistent with or contrary to data and observations to date, including that later data may not indicate a patient benefit, modulate toxicities or validate a mechanism of action; (10) inaccuracy in the Company's estimates regarding expenses, future revenue, capital requirements and needs for and the ability to obtain additional financing; (11) the Company's ability to protect and enforce its intellectual property portfolio, including any newly issued patents and its ability to obtain any expected patent term extensions, adjustments, exclusivities or disclaimers; and (12) other risks and uncertainties indicated from time to time in the Company's filings with the U.S. Securities and Exchange Commission (the "SEC"), including the risks and uncertainties described in the "Risk Factors" section of the Company's most recent Annual Report on Form 10-K filed with the SEC on January 30, 2026 and subsequently filed reports. Forward-looking statements contained in this announcement are made as of this date, and the Company undertakes no duty to update such information except as required under applicable law.

Investor Contact:
JTC Team, LLC
Jenene Thomas
(908) 824-0775
GRI@jtcir.com

FAQ

What type of study was GRI-0621-IPF-02 and how was it designed?

GRI-0621-IPF-02 was a randomized, double-blind, placebo-controlled Phase 2a trial in idiopathic pulmonary fibrosis. Thirty-five patients were randomized 2:1 to receive GRI-0621 4.5 mg once daily (23 patients) or placebo (12 patients) for 12 weeks, with 80% of participants on background pirfenidone or nintedanib. Safety was the pre-specified primary endpoint, with translational biomarkers and FVC as exploratory measures.

What are the nine mechanistic pillars identified for GRI-0621 in IPF?

The data supported nine pre-specified mechanistic pillars for GRI-0621 in IPF: immune re-balancing, reduced lung injury, myofibroblast inhibition, fibrolysis, basement-membrane repair, re-epithelialization, FVC stabilization, antitussive effect and gastrointestinal protection. Each pillar was supported by direction-consistent signals from at least two of four measurement modalities.

Which biomarker modalities were integrated to characterize GRI-0621’s mechanism of action?

The analysis integrated four modalities from the same patient population: whole-blood RNA sequencing of 72 anchor genes, an expanded 12-marker serum extracellular matrix neo-epitope panel, 28-color spectral flow cytometry of paired blood and bronchoalveolar lavage, and clinical and patient-reported readouts. Concordant signals across these modalities underpinned the mechanistic pillars.

How did GRI-0621 affect cough and gastrointestinal side effects compared with placebo?

Treatment-emergent cough occurred in 0% of GRI-0621-treated patients versus 25% on placebo. Diarrhea occurred in 17% on GRI-0621 versus 33% on placebo, and weight loss in 0% versus 17%, despite higher background nintedanib use in the GRI-0621 arm. These findings align with antitussive and GI-protective mechanistic signals.

Where and how were these Phase 2a data for GRI-0621 presented?

The findings were presented at the 2026 European Respiratory Society Congress in Barcelona as a late-breaking oral presentation and three posters covering safety, translational biomarkers, and lung function in the GRI-0621-IPF-02 study.