Expedition Raises $115M for a China-Licensed COPD Pill Targeting Inflammation

Expedition Therapeutics has raised $115 million to develop a once-daily pill for chronic obstructive pulmonary disease (COPD), one of the world’s leading causes of death.

The Series B, announced August 5, 2026, was led by General Atlantic and joined by Vivo Capital, RA Capital, Forbion, Sofinnova, Novo Holdings, Venrock and others. It brings total funding to nearly $300 million, following a $165 million Series A. General Atlantic’s Brett Zbar joins the board.

What DPP1 does

Lead candidate EXPD-101 (originally XH-S004) is a DPP1 inhibitor — it blocks dipeptidyl peptidase-1, an enzyme upstream of the inflammation that drives COPD.

The upstream position is the whole design rationale. DPP1 does not itself damage tissue. Its job is to activate a group of destructive enzymes — neutrophil serine proteases including neutrophil elastase — while neutrophils are still maturing in the bone marrow.

Those proteases are what actually break down lung tissue when neutrophils release them at sites of inflammation. Blocking DPP1 means neutrophils enter circulation without functional proteases loaded — so the cells still arrive and respond, but arrive disarmed.

Why that is a better target than the proteases themselves

Attempts to inhibit neutrophil elastase directly have a long and disappointing history.

The difficulty is redundancy: several related proteases perform overlapping functions, so blocking one leaves others operating. Achieving sustained inhibition at the site of release, where local concentrations are extremely high, has also proved hard.

Acting one step earlier addresses both problems at once. A single enzyme activates the whole family, so inhibiting it reduces all of them, and it acts in the bone marrow rather than in inflamed tissue — a more accessible compartment with more predictable drug exposure.

Why COPD needs this

“You take this pill once a day, and it can target that underlying inflammation that all the COPD patients have,” said CEO Yi Larson.

Existing COPD treatment is largely symptomatic. Bronchodilators relax airway muscle, improving airflow without affecting the disease process. Inhaled corticosteroids reduce inflammation broadly and work better in some patients than others, with pneumonia risk as a recognised cost.

Neither stops the progressive tissue destruction that defines the disease. Lung function declines regardless, and the damage does not reverse — which is why an agent targeting the destructive mechanism is a different proposition from another symptomatic option.

The neutrophil trade-off

Disarming neutrophils raises an obvious question, since those proteases exist to kill bacteria.

DPP1 inhibition has been studied in bronchiectasis, a related condition of chronic neutrophilic airway inflammation, where the approach showed benefit in reducing exacerbations. Infection risk is the parameter that requires careful monitoring in any such programme.

The favourable consideration is that COPD patients already suffer frequent infective exacerbations, partly because chronic inflammation and damaged airways impair clearance. Whether reducing protease-mediated damage improves that balance or worsens it is precisely what a Phase 2 trial must establish.

Licensed from China

The drug was licensed from China’s Fosun Pharma, with Expedition holding global rights outside certain territories. The deal reflects a broader trend of Western biotechs licensing promising, lower-cost candidates out of China.

The pattern recurs because the economics are favourable on both sides: the originator monetises an asset in markets it cannot easily reach, and the licensee acquires a clinical-stage programme for less than developing one costs.

What comes next

Expedition has begun recruiting for what it calls the first global Phase 2 trial of a DPP1 inhibitor in COPD, with initial data expected in 2028.

Why COPD trials are structurally difficult

The disease presents design problems that have defeated several well-supported programmes, and they shape what Expedition’s Phase 2 can realistically show.

COPD is heterogeneous. The label covers patients whose disease is driven predominantly by emphysema — destruction of lung tissue — and others whose problem is chronic bronchitis with mucus and airway inflammation, plus many with both. A drug targeting neutrophilic inflammation should help some of those patients considerably more than others.

Enrolling broadly therefore dilutes any effect. Enrolling narrowly requires a way to identify the right subgroup, and biomarkers for neutrophilic COPD exist but are imperfect and not routinely measured.

Progression is also slow. Lung function declines by a small amount each year, so demonstrating that a drug slows it requires large numbers followed for years — which is why exacerbation frequency has become the practical endpoint, despite being influenced by infections, air quality and adherence as much as by the underlying disease.

COPD already has several approved therapies, so EXPD-101 will need to show it can meaningfully improve on them — and the endpoint chosen will shape that. Exacerbation reduction is achievable in a Phase 2 timeframe; demonstrating slowed decline in lung function requires years, and it is the claim that would distinguish a disease-modifying drug from a better symptomatic one. Business news, not investment or medical advice.