Gossamer Bio : Q1 2026 Earnings Call Presentation (6f49a5)

Published: 2026-05-18 08:37:06 ET GOSS

Published on 05/18/2026 at 08:37 am EDT

May 2026

Faheem Hasnain, Co-Founder, Chairman & Chief Executive Officer

Bryan Giraudo, Chief Operating Officer & Chief Financial Officer

Bob Smith, Chief Commercial Officer

Caryn Peterson, Executive Vice President, Regulatory Affairs

Dr. Rob Roscigno, Senior Vice President, Clinical Development, Pulmonary Vascular Disease

Dr. Jean-Marie Bruey, Senior Vice President, Translational Medicine and Research

Dr. Rainer Zimmermann, Vice President, Medical Affairs

Dr. Megan Flynn, Vice President, Medical Affairs

Dr. Robin Osterhout, Executive Director, Translational Medicine

FDA has confirmed an in-person meeting for Mid-June

Meeting will address the regulatory path forward for seralutinib, including discussion of the totality of clinical evidence across the clinical program

Subject to a productive Type B meeting outcome, Gossamer is targeting an NDA submission in September 2026

We expect to submit an NDA under the basis of one adequate and well-controlled clinical investigation (PROSERA) plus confirmatory evidence (TORREY), supported by the seriousness of PAH, high unmet need, and seralutinib's novel mechanism of action

PROSERA CT FRI Substudy:

Most Comprehensive Controlled Vascular Imaging Dataset in PAH to Date

Clinical endpoints show whether patients improved; computed tomography functional respiratory imaging (CT FRI) reveals the anatomical basis of that improvement, which is key for a non-vasodilator

Built on seralutinib's initial arterial reverse remodeling signal seen in Phase 2 TORREY CT FRI substudy (n=19); the

PROSERA CT FRI substudy was designed to further validate this treatment effect

We believe this to be the largest and most comprehensive CT FRI dataset from a controlled therapeutic trial in PH: 162 enrolled, 125 paired scans at Week 24, in patients on multiple concurrent background PAH vasodilators

Prespecified exploratory substudy using an updated algorithm with improved proximal large-vessel capture versus TORREY

Substudy was representative of the broader PROSERA intent-to-treat (ITT) (n=390) on demographics, hemodynamics, and risk profile

Week 24 clinical endpoints in the substudy were consistent with the broader ITT population

FRI = functional respiratory imaging; CT = computed tomography; 6MWD = 6-minute walk distance; NT-proBNP = N-terminal pro-B-type natriuretic peptide; ITT = intent-to-treat; REVEAL Lite 2 = Registry to Evaluate Early and Long-Term PAH Disease Management 7

Lite 2 risk score.

Baseline

Week 24

Seralutinib Patient Case Study:

Visualization of Reverse Remodeling

Prespecified imaging endpoints showed statistically significant, multi-compartment effects of seralutinib across arterial, venous, and fibrosis-like parenchymal parameters

The breadth and internal consistency of these effects exceed prior controlled PAH imaging data, including TORREY's arterial-only signal

Imaging changes correlated more tightly with clinical endpoints (including 6MWD, NT-proBNP, REVEAL Lite 2) than in TORREY, reinforcing clinical relevance

Pattern is biologically coherent and consistent with seralutinib's platelet-derived growth factor receptor (PDGFR) + colony stimulating factor 1 receptor (CSF1R) + c-KIT mechanism of action

Substudy was prespecified as exploratory; all p-values are nominal and unadjusted for multiplicity

Color indicates vessel cross sectional area. Red denotes small-caliber vessels; blue denotes large-caliber vessels. Redistribution from blue to red is consistent with reverse remodeling. Individual result; treatment effects vary by patient.

6MWD = 6-minute walk distance; NT-proBNP = N-terminal pro-B-type natriuretic peptide; PDGFR = platelet-derived growth factor receptor; CSF1R = colony stimulating factor 1 receptor; REVEAL Lite 2 = Registry to Evaluate Early and Long-Term PAH Disease 8

Management Lite 2 risk score; c-KIT = mast/stem cell growth factor receptor.

PAH Is a Multi-Compartment Vascular Disease, Not Just Arterial Remodeling

Pulmonary Veins

Capillary Bed

Pulmonary Arteries

PAH is a multi-compartment disease including:

Arterial remodeling

Capillary dropout

Deoxygenated Blood Flow

Gas Exchange

Oxygenated Blood Flow

Venous underfilling

Venous underfilling reflects reduced transpulmonary flow (not venous disease)

Volumes are reduced in PAH;(1) consistent with downstream flow impairment

CT FRI measurable

Precapillary arteriolar lesions and parenchymal fibrosis converge on the capillary bed, below CT resolution

Damage here is a major driver of clinical decline

Inhaled seralutinib deposits in alveoli and penetrates to capillary bed

PDGFR signaling thickens artery walls and narrows the vessels

Reversal of this process is consistent with redistribution from larger to smaller arteries

CT FRI measurable

Perivascular fibrosis

Inflammation

FRI captures sections of an integrated arterial - capillary - venous system and the surrounding parenchymal space

Parenchymal remodeling with fibrotic-like features contributes to vascular stiffening; macrophage infiltration and fibrous tissue buildup drive tissue density changes detectable by CT

Parenchymal Space

Changes in one compartment (whether positive or negative) propagate to others

CT = computed tomography; FRI = functional respiratory imaging; PDGFR = platelet-derived growth factor

receptor. 9

1) Rahaghi FN et al. Chest 2021;160(6):2220-2231

Pulmonary Arteries

Parenchymal Space

Pulmonary Veins

PAH

& Seralutinib

PDGFRα/β

→

PASMC proliferation

→

Medial hypertrophy

→

Seralutinib inhibits PDGFRα/β

→

Redistribution from large arteries to small arteries

PDGFRα/β (fibroblasts)

+ CSF1R (macrophages)

+ c-KIT (mast cells)

→

Fibroblast activation, inflammation, and

parenchymal remodeling

→

Seralutinib inhibits PDGFRα/β + CSF1R + c-KIT

→

Decreased fibrosis-like parenchymal features

Upstream arterial remodeling + anti-fibrotic effects

(incl. sub-CT capillary bed)

→

Improved transpulmonary flow

→

Venous recovery

Seralutinib CT FRI

Treatment Effect in PROSERA

v. Placebo

Large arterial blood volume

proportion ↓

(BV10A%, p=0.020)

Fibrosis-like parenchymal volume ↓

(FV, p=0.026)

Normalized fibrosis-like

volume↓

(FVN, p=0.025)

Total venous volume ↑

(TVV, p=0.016)

Small venous blood volume ↑ (BV5V, p=0.034) (BV510V, p=0.041)

Venous fractal dimension ↑

(FDOPV, p=0.044)

CT = computed tomography; FRI = functional respiratory imaging; PDGFRα/β = platelet-derived growth factor receptor alpha/beta; PASMC = pulmonary artery smooth muscle cell; CSF1R = colony stimulating factor 1 receptor; BV10A% = arterial vessel volume >10 mm² as proportion of total blood volume; FV = fibrosis volume; FVN = normalized fibrosis volume (FV/lung volume); TVV = total venous blood volume; BV5V = venous vessel volume <5 mm²; BV510V = venous vessel volume 5-10 mm²; FDOPV = fractal dimension of pulmonary venous vessels; IPF = idiopathic pulmonary fibrosis; HAA = High Attenuation Area. All p-values are nominal and unadjusted for multiplicity.

FRI fibrosis volume (FV) quantifies CT voxel-level features characteristic of fibrotic tissue, derived from a deep-learning algorithm (FibroNet) trained on confirmed IPF patient datasets. Methodologically analogous to the High Attenuation Area (HAA)

BV10A% Clinical Correlations (p<0.05)

At baseline: correlated with PVR, mPAP, NT-proBNP, ESC/ERS risk

Change at 24 Weeks: correlated with 6MWD, NT-proBNP, REVEAL Lite 2, ESC/ERS risk

Seralutinib significantly decreased large arterial blood volume proportion (BV10A%) v. placebo, indicating of proximal arterial decompression

Consistent with TORREY arterial results, now reproduced in a much larger population

BV10A% demonstrated among the strongest clinical correlations of any FRI parameter

Changes at 24 weeks correlated with improvements across multiple clinical endpoints

Seralutinib Decreased BV10A%

BV10A% = arterial vessel volume >10 mm² as proportion of total blood volume; 6MWD = 6-minute walk distance; NT-proBNP = N-terminal pro-B-type natriuretic peptide; REVEAL Lite 2 = Registry to Evaluate Early and Long-Term PAH Disease Management Lite 2 risk 11

score; ESC/ERS = European Society of Cardiology / European Respiratory Society risk strata; PVR = pulmonary vascular resistance; mPAP = mean pulmonary arterial pressure; TORREY = Phase 2 trial of seralutinib in PAH.

Rahaghi FN et al. Chest 2021;160(6):2220-2231. All p-values are nominal and unadjusted for multiplicity.

Seralutinib Reduces Fibrosis-Like Parenchymal Features While Placebo Increases

Seralutinib Decreased Fibrosis-like Volume Metric

Seralutinib significantly decreased functional respiratory imaging (FRI) fibrosis metrics

(1), placebo increased

First demonstration of statistically significant fibrotic reduction in controlled PAH trial

Decreases seen across subgroups, including non-connective tissue disease (CTD)

patients

Reduction in fibrosis-like parenchymal features is consistent with PDGFR, CSF1R and c-KIT pathway inhibition, an antifibrotic effect distinct from vasodilation

The same fibrotic and inflammatory pathobiology drives PH-ILD and other fibrotic lung diseases, supporting the potential relevance of seralutinib beyond PAH

Fibrotic Metrics' Clinical Correlations (p<0.05)

At baseline: correlated with NT-proBNP, ESC/ERS risk

Change at 24 Weeks: correlated with NT-proBNP, REVEAL Lite 2

FRI = functional respiratory imaging; FV = fibrosis volume; CT = computed tomography; NT-proBNP = N-terminal pro-B-type natriuretic peptide; ILD = interstitial lung disease; IPF = idiopathic pulmonary fibrosis; CTD = connective tissue disease; FVN = normalized fibrosis volume; ESC/ERS = European Society of Cardiology / European Respiratory Society; REVEAL Lite 2 = Registry to Evaluate Early and Long-Term PAH Disease Management Lite 2 risk score; CSF1R = colony stimulating factor 1 receptor; c-KIT = KIT proto-oncogene receptor tyrosine kinase; PH-ILD = pulmonary hypertension-interstitial

lung disease. 12

FRI fibrosis volume (FV) quantifies CT voxel-level features characteristic of fibrotic ILD (e.g., reticulation, ground-glass), derived from FibroNet deep-learning algorithm trained on confirmed IPF patient datasets.

Osterhout et al, AJRCCM, Accepted (2026)

Venous Fractal Dimension (FDOPV; p=0.0435)

Increased vascular branching

Increased venous branching complexity suggests structural vascular recovery, not merely passive volume redistribution

Consistent with attenuation of vascular pruning, a

hallmark of progressive PAH1

In the PROSERA substudy, seralutinib significantly increased venous blood

volume; placebo decreased

Consistent increases across venous vessel sizes and vascular branching (fractal dimension), suggesting improved microvascular flow and perfusion

Venous volumes and vascular branching correlated with PVR and cardiac output at baseline (p<0.05, Spearman)

Venous improvements likely capture the totality of upstream treatment effects, including arterial, anti-fibrotic, and sub-CT capillary bed changes

First demonstration of venous vascular recovery in a controlled PAH trial

Venous Clinical Correlations (p<0.05)

At baseline: venous volumes correlated with PVR and cardiac output; BV510V also correlated with FEV1 and FVC; FDOPV correlated with cardiac output

Change at 24 Weeks: BV10V correlated with REVEAL Lite 2; FDOPV correlated with FEV1

TVV = total venous blood volume; BV5V = venous vessel volume <5 mm²; BV510V = venous vessel volume 5-10 mm²; BV10V = venous vessel volume >10 mm²; FDOPV = fractal dimension of pulmonary venous vessels; CT = computed tomography; FRI = functional 13

respiratory imaging; PVR = pulmonary vascular resistance; FEV1 = forced expiratory volume in 1 second; FVC = forced vital capacity.

Functional Respiratory Imaging (FRI) Links Vascular Structure to Clinical Trajectory in PAH

At baseline, arterial, venous, and vascular complexity parameters correlated with pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), cardiac output, and clinical outcome measures (N=156), relationships not detectable in TORREY substudy

Furthermore, changes in FRI parameters correlated with improvements in 6MWD, NT-

proBNP, and risk scores, linking structural imaging findings to clinical benefit

This supports FRI as a biologically and clinically relevant readout in PAH, anchoring the treatment-effect data

Arterial Correlations

Correlations with Baseline Characteristics

+: p < 0.05

++: p < 0.01

+++: p < 0.001

Venous Correlations

Correlations with Baseline Characteristics

+: p < 0.05

++: p < 0.01

+++: p < 0.001

PVR

MPAP

NT-

proBNP

REVEAL

Lite 2

ESC/

ERS

FEV1

FVC

BV5A/BV10A

+++

BV5A%

BV10A%

+++

PVR

FEV1

FVC

TVV

BV10V

+++

BV510V

+++

BV5V

FDV

FRI = functional respiratory imaging; PVR = pulmonary vascular resistance; mPAP = mean pulmonary arterial pressure; NT-proBNP = N-terminal pro-B-type natriuretic peptide; REVEAL Lite 2 = Registry to Evaluate Early and Long-Term PAH Disease Management Lite 2 risk score; ESC/ERS = European

Society of Cardiology / European Respiratory Society; CO = cardiac output; 6MWD = 6-minute walk distance; FEV1 = forced expiratory volume in 1 second; FVC = forced vital capacity; BV5A = arterial vessel volume <5 mm²; BV10A = arterial vessel volume >10 mm²; BV5A% = arterial vessel volume <5

mm² as proportion of total blood volume; BV510V = venous vessel volume 5-10 mm²; BV5V = venous vessel volume <5 mm²; TVV = total venous blood volume; BV10V = venous vessel volume >10 mm²; FDV = fractal dimension of venous vessels. 14

1) Rahaghi et al. Chest 2021;160(6):2220-2231

All correlations at baseline, pooled across treatment arms.

Seralutinib Demonstrated Statistically Significant Treatment Effects Across Multiple Vascular Compartments

Category

Parameter

Abbrev.

Effect

p-value

Interpretation

Arterial

Arterial vessel volume >10mm² / TBV

BV10A%

↓ Decrease

0.020*

Reduced proportion of large-artery volume consistent with proximal decompression

Arterial

Arterial vessel volume >10mm²

BV10A

↓ Decrease

0.230

Reduced large-artery volume

Arterial

Small / large arterial vessel ratio

BV5A/BV10A

↑ Increase

0.556

Shift in arterial volume toward smaller vessels

Arterial

Arterial vessel volume <5mm²

BV5A

↑ Increase

0.660

Increased small-vessel arterial volume

Parenchymal

Fibrosis-like parenchymal volume

↓ Decrease

0.026*

Reduced fibrosis-like parenchymal volume

Parenchymal

Normalized fibrosis-like parenchymal volume

FVN

↓ Decrease

0.025*

Reduced proportion of fibrosis-like volume

Venous

Total venous blood volume

TVV

↑ Increase

0.016*

Increased venous filling; placebo decreased

Venous

Venous vessel volume <5mm²

BV5V

↑ Increase

0.034*

Increased small venous vessel volume

Venous

Venous vessel volume 5-10mm²

BV510V

↑ Increase

0.041*

Increased mid-size venous vessel volume

Venous

Venous vessel volume >10mm²

BV10V

↑ Increase

0.188

Increased large venous vessel volume

Venous

Fractal dimension of venous vessels

FDOPV

↑ Increase

0.044*

Increased vascular branching

TBV = total blood volume; 6MWD = 6-minute walk distance; FDOPV = fractal dimension of pulmonary venous vessels; BV5VPR = venous vessel volume <5mm² / total blood volume; SAP = statistical analysis plan; FRI = functional respiratory imaging; CT = computed tomography. In addition to the 7 nominally statistically significant prespecified parameters shown above, BV5VPR (venous vessel volume <5mm² / TBV) also achieved nominal significance (p=0.020). Prespecified exploratory parameters per SAP v2.1; p-values are nominal and unadjusted for multiplicity. Clinical correlations shown are Spearman, segregated as baseline vs. Δ, pooled across both arms, and are descriptive rather than confirmatory. FRI fibrosis volume (FV) quantifies CT voxel-level features characteristic of 15

fibrotic tissue, derived from a deep-learning algorithm (FibroNet) trained on confirmed IPF patient datasets. * denotes statistical significance.

Two Patients on Triple Background Therapy, Two Trajectories:

Visualization of Reverse Remodeling (Placebo v. Seralutinib)

Placebo patient

Seralutinib patient

Baseline

Week 24

Baseline

Week 24

60y Female, PAH-CTD, FC 3, Triple Therapy

Δ 6MWD

-1 m

Δ NT-proBNP

-143 ng/L

Δ BV10A, BV5A

+12.6 mL, -6.8 mL

Δ Total Venous Volume

-8.9 mL

70y Female, IPAH, FC 3, Triple Therapy

Δ 6MWD

+55 m

Δ NT-proBNP

-324 ng/L

Δ BV10A, BV5A

-4.2 mL, +5.5 mL

Δ Total Venous Volume

+8.8 mL

IPAH = idiopathic pulmonary arterial hypertension; CTD = connective tissue disease; FC = functional class; 6MWD = 6-minute walk distance; NT-proBNP = N-terminal pro-B-type natriuretic peptide; BV10A = arterial vessel volume >10 mm²; BV5A =

arterial vessel volume <5 mm².

Individual patient data are illustrative and not representative of the overall study population.

Baseline

Week 24

Reduced Fibrosis-like

CT features

Fibrosis volume (FV) quantified via FibroNet, a deep-learning algorithm trained on confirmed idiopathic pulmonary fibrosis (IPF) data (analogous to High Attenuation Abnormalities [HAA] in ILD imaging)

Seralutinib patient

54yo female, IPAH, FC 3, Double Therapy

Δ 6MWD

+73m

Δ NT-proBNP

-307 ng/L

Δ FV

-64.7 mL

Δ FVN

-1.64

CT detects fibrotic changes only around larger vessels; true parenchymal remodeling burden is likely underestimated, especially in the sub-CT-resolution capillary bed

Consistent with seralutinib's PDGFR / CSF1R / c-KIT mechanism: fibroblast, macrophage and mast cell remodeling inhibition, reflected as reduced parenchymal density on CT

FV = fibrosis volume; FVN = normalized fibrosis volume; CT = computed tomography; FRI = functional respiratory imaging; PDGFR = platelet-derived growth factor receptor; CSF1R = colony stimulating factor 1 receptor; c-KIT = KIT proto-oncogene receptor tyrosine kinase; HAA = High Attenuation Abnormalities; ILD = interstitial lung disease; IPF = idiopathic pulmonary fibrosis; PH-ILD = pulmonary hypertension-interstitial lung disease; IPAH = idiopathic pulmonary arterial hypertension; FC = functional class;

6MWD = 6-minute walk distance; NT-proBNP = N-terminal pro-B-type natriuretic peptide. FRI fibrosis volume (FV) quantifies CT voxel-level high-attenuation features characteristic of fibrotic tissue. All p-values are nominal and unadjusted for multiplicity. 17

Individual patient images are illustrative and not representative of the study population.

Multi-compartment vascular and parenchymal remodeling effects of this breadth have not been shown by traditional vasodilator therapies

First controlled-trial imaging evidence of arterial decompression with concomitant venous vascular expansion, indicating coordinated restoration of pulmonary vascular flow

Imaging and clinical results point to a mechanism-based effect on PAH disease biology, not just symptomatic

relief, consistent with PDGFRα/β + CSF1R + c-KIT pathway inhibition

Imaging results correlated with improvements in 6MWD, NT-proBNP, and REVEAL Lite 2, linking structural remodeling to clinical benefit

Seralutinib's mechanism of action may extend to fibrotic lung diseases, particularly those with a pulmonary

vascular component

These data strengthen the cumulative weight of evidence for seralutinib, extending the consistent signal seen across the program's clinical trials: the placebo-controlled Phase 1b, the Phase 2 TORREY Study, and the Phase 3 PROSERA Study

PDGFRα/β = platelet-derived growth factor receptor alpha/beta; CSF1R = colony stimulating factor 1 receptor; c-KIT = KIT proto-oncogene receptor tyrosine kinase; 6MWD = 6-minute walk distance; NT-proBNP = N-terminal pro-B-type natriuretic peptide; REVEAL Lite 2 = Registry to Evaluate Early and Long-Term PAH Disease Management Lite 2 risk score. Note: all significance calculations are nominal and unadjusted for multiplicity.

Existing Notes

$200mm, 5.00% Convertible Senior Notes due 2027

Exchange Consideration

Per $1,000 principal: up to 1,588.2353 shares of common stock (or pre-funded warrants in lieu

thereof) + $360 principal amount of new secured notes + 750 early tender purchase warrants

New Notes

7.50% Senior Secured First Lien Convertible Notes due 2030

Debt Reduction(1)

$200mm → $72mm (would reduce debt by $128mm, or 64%)

Maturity Extension(1)

2027 → 2030

Strategic Rationale

Addresses near term capital structure overhang

Noteholder Support

75% of existing noteholders have entered into a Transaction Support Agreement

(1) Assumes 100% participation. 20

Disclaimer

Gossamer Bio Inc. published this content on May 18, 2026, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on May 18, 2026 at 12:36 UTC.