Lusupultide
A lab-made copy of lung surfactant protein C, mixed with lipids as Venticute and given into the airways of adults with ARDS in five trials that improved oxygen levels but not survival
Lusupultide is recombinant surfactant protein C (rSP-C): a 34-residue copy of the human SP-C protein with three amino acids changed, mixed with phospholipids and palmitic acid to form the surfactant Venticute. Trials published from 2003 to 2011 enrolled about 1,400 adults with acute respiratory distress syndrome or severe pneumonia, roughly half of whom received it through the breathing tube. Oxygen levels improved in the early trials, but no trial showed that it saved lives, and it was never approved.
Used in human trials: 50 mg/kg per dose, Up to 4 doses, Intratracheal, through the breathing tube (Study: ARDS, pooled analysis of five trials) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
The air sacs of the lung are lined with a thin film called surfactant, a mixture of phospholipids and a few proteins that lowers surface tension so the sacs stay open. Natural surfactants taken from cattle contain two small proteins, SP-B and SP-C, and in rat tests the lipids alone worked far less well than the same lipids with SP-C added (PMID 9655740). Premature babies lack surfactant, and their respiratory distress syndrome is treated with a breathing machine and surfactant given down a tube (PMID 19649338). Adults with acute respiratory distress syndrome (ARDS) have surfactant too, but its composition and function are badly disturbed (PMIDs 17287298, 21148720), which raised the question of whether topping it up would help them as well.
Lusupultide is a recombinant version of SP-C rather than one extracted from animal lungs: the 34-residue human sequence with the two cysteines at positions 4 and 5 replaced by phenylalanine and the methionine at 32 replaced by isoleucine (PMID 9609732). Mixed with dipalmitoylphosphatidylcholine, phosphatidylglycerol and palmitic acid it became the suspension called rSP-C surfactant, later Venticute (PMID 10658037). Its early animal work came from the German company Byk Gulden (PMID 9655740), the pooled trial analysis from Nycomed (PMID 18689599), and the last trial was sponsored by Takeda (NCT00074906).
In animals the drug behaved like a natural surfactant. In rats whose lungs had been washed free of their own surfactant, it raised blood oxygen in step with the dose and limited the hyaline membranes that form in injured lungs, about as well as bovine extracts and far better than the same lipids without the protein (PMIDs 9655740, 9720777, 10419839). It also worked in lavaged sheep and pigs (PMIDs 10051245, 10658037), in premature lambs and rabbits (PMIDs 9476872, 16763385), in piglets after meconium aspiration (PMIDs 12955179, 16374175) and in rabbits after aspirating acidified infant formula (PMID 15105199). In the laboratory it resisted inactivation by meconium better than several animal-derived surfactants (PMID 11420417).
The human programme ran in adults with ARDS. A North American phase I/II trial found it well tolerated but without clear benefit (PMID 12649125), and a European pilot showed better gas exchange and a near-normal surfactant composition in lung washings, though the material's surface activity recovered only partly (PMID 17287298). Two phase 3 trials in 448 patients, published in 2004, found that up to four doses in 24 hours improved oxygenation during treatment but did not change survival or time on the ventilator (PMID 15329426).
A pooled analysis of all five trials, 532 patients in total, confirmed the oxygen gain and the lack of any overall effect on deaths, but found that patients whose ARDS came from pneumonia or aspiration seemed to live longer when treated, a post-hoc finding (PMID 18689599). That hypothesis was tested in 843 patients with severe pneumonia or aspiration at 161 centres, using up to eight doses over 96 hours. The trial found no benefit on any outcome, not even oxygenation, and the investigators traced the problem to a new step in preparing the suspension that appears to have partly inactivated the drug (PMID 21148720). No further human trials have been published.
Later work turned to inhaling the surfactant as a dry powder, which could deliver large amounts without filling the lungs with liquid. A powder aerosolizer restored lung function in rabbits and mice (PMID 20400897), and a humidified version was built for preterm babies breathing through nasal prongs (PMID 23421901), but neither reached a published human trial. Lusupultide is not the same as lucinactant, another synthetic surfactant, whose peptide sinapultide imitates surfactant protein B rather than C and which was briefly approved for premature babies.
Mechanism of Action
Lusupultide does nothing as a free protein; its job is to make a lipid film spread and hold at the air-water surface of the air sacs. The animal and human studies point to a physical effect on surface tension and gas exchange, and a smaller, less certain effect on inflammation.
Surface tension
With its lipids it lowers surface tension at the air-sac lining, which keeps the sacs open and improves oxygen uptake; the same lipids without the protein work far less well (PMIDs 9655740, 9476872).
Resisting inactivation
It withstood meconium better than several animal surfactants in the laboratory (PMID 11420417), but neutral lipids that build up in ARDS lungs weakened it (PMID 17287298).
Fewer hyaline membranes
In lavaged rats it limited the protein-rich membranes that line injured air sacs, more so with dexamethasone, roflumilast or a COX inhibitor added (PMIDs 10598681, 10715602, 10806144).
Clearance
The lung clears it at the same pace as native SP-C and its main lipid, with a half-life of about 11 hours in rabbits (PMIDs 9609732, 9853918).
Published Research
These are studies of lusupultide, the recombinant SP-C, given in its phospholipid surfactant (rSP-C surfactant, Venticute), read from their PubMed abstracts: the five human trials and their pooled analysis, laboratory tests on human cells, and animal studies in rats, rabbits, sheep, pigs, lambs, piglets and guinea pigs. Studies of other recombinant or synthetic SP-C molecules are listed under References only.
First North American trial
In a phase I/II trial, adults with ARDS were randomised to usual care or usual care plus the rSP-C surfactant at one of two dose levels, each given four times in 24 hours. The instillations were well tolerated but brought no measurable clinical benefit. Lung washings at 48 hours held the drug's components and less interleukin-6 than controls, a sign of reduced inflammation, yet their surface tension was no better; by 120 hours the drug could no longer be detected. The authors suggested larger doses for longer.
Two phase 3 trials in ARDS
In two double-blind multicentre trials, 448 adults with ARDS of many causes received usual care alone or usual care plus up to four doses of the surfactant into the airway within 24 hours. Survival at 28 days was 66% overall and did not differ between groups, and neither did time on the ventilator. Blood oxygen levels improved more with the surfactant during the 24-hour treatment window, which led the investigators to propose a longer course.
What happens to the lung's own surfactant
In a randomised pilot trial of 31 patients with ARDS given the surfactant into the bronchi, gas exchange improved and the make-up of phospholipids and proteins in lung washings came close to normal, but the ability of that material to lower surface tension recovered only partly. ARDS lungs carried about twice the normal amount of neutral lipids, and adding such lipids to the drug in the laboratory weakened it in a dose-dependent way, one possible reason for the limited effect.
Pooled analysis of five trials
Pooling all five multicentre trials, 266 patients given up to four airway doses of 50 mg/kg were compared with 266 on usual care. Oxygenation improved with treatment, but death rates did not change (32.6% overall). Age and APACHE II score predicted death most strongly. In a post-hoc subgroup with severe ARDS caused by pneumonia or aspiration, treated patients had better oxygenation and better survival, a finding that set up the next trial.
Severe pneumonia and aspiration: no benefit
The confirmatory trial (NCT00074906) ran at 161 centres in 22 countries: 419 patients with severe direct lung injury from pneumonia or aspiration received usual care plus up to eight doses over 96 hours, and 424 received usual care. Mortality at 28 days, time on the ventilator and days free of other organ failure were the same in both groups, and unlike earlier trials oxygenation did not improve. Investigators traced the failure to a new step in preparing the suspension that appears to have partly inactivated the drug.
Resistance to meconium
On a pulsating bubble surfactometer, human meconium was mixed with eight surfactants at 2.5 mg/mL. The rSP-C surfactant (Venticute) lost its ability to reach low surface tension only at meconium levels of 0.32 mg/mL or more, against 0.04 mg/mL for the animal-derived Curosurf, Alveofact and Survanta, so it was more resistant than those; natural lavage surfactant containing SP-A was the most resistant of all.
Human monocytes and inflammatory signals
In THP-1 human monocyte cells stimulated with bacterial endotoxin, both Venticute and the pig-derived Curosurf lowered the rise in TNF-alpha messenger RNA. Venticute raised the anti-inflammatory IL-10 signal somewhat more, and unlike Curosurf it did not increase IL-8 at higher concentrations.
Eosinophils from allergic volunteers
Blood eosinophils from atopic volunteers were incubated with Curosurf, Alveofact or Venticute for up to 42 hours. Venticute briefly raised the share of dying cells at one hour, with no difference later; all three preparations increased release of eosinophil cationic protein at 20 hours. Only Curosurf made the cells' fluid more attractive to other eosinophils, so the pig surfactant looked the most pro-inflammatory of the three.
A powder aerosolizer for preterm babies
Engineers described a continuous device that turns dry rSP-C surfactant powder into a dense, humidified aerosol for delivery through nasal prongs, aiming to spare preterm infants a breathing tube. It produced a flow of about 0.84 L/min carrying up to 12 g of surfactant per cubic metre, with wet particles of 3 to 3.5 micrometres at the patient end, and had been used in preclinical work.
How fast the lung clears it
Iodine-labelled rSP-C, the 34-residue human sequence with phenylalanine at positions 4 and 5 and isoleucine at 32, was instilled into rabbit and mouse airways. In rabbits it left the lung with a half-life of about 11 hours, the same as native SP-C and the main lipid DPPC; in mice it lingered longer (28 hours against 12 for DPPC). Lung cells in culture took it up much as they take up the native protein.
Clearance in premature lambs
In preterm lambs given trace amounts at birth, only 8.3% of labelled rSP-C and 14.7% of labelled DPPC remained in the air spaces after two hours, and about a fifth of the rSP-C had left the lungs altogether. At a treatment dose of 100 mg/kg, rSP-C and DPPC were recovered from the air spaces and lung tissue in equal proportions after five hours of ventilation.
Premature lambs and rabbits
In the laboratory the rSP-C surfactant lowered surface tension further than natural sheep surfactant and was just as sensitive to inhibition by plasma. Preterm lambs given 100 mg/kg at birth did as well over five hours as those given natural surfactant on carbon dioxide levels, lung mechanics and lung volume, and preterm rabbits showed similar compliance gains. Surfactant washed back out of treated lambs still worked when tested again.
Rat lavage model: dose response
Rats whose lungs were washed free of surfactant were treated an hour later with 25, 50 or 100 mg phospholipid/kg. Arterial oxygen two hours on reached 318, 443 and 480 mm Hg with the rSP-C surfactant against roughly 100 to 130 with the same lipids lacking the protein, and 74 in untreated rats. Only surfactants containing protein reduced hyaline membranes with rising dose, and the rSP-C product matched the bovine extracts tested.
Late treatment against seven surfactants
When treatment was delayed for an hour after lavage, the protein-containing surfactants (rSP-C surfactant, bLES, Infasurf and Survanta) all raised oxygen in a dose-dependent way at 30 minutes, while protein-free products such as Exosurf and ALEC did little. By two hours only the rSP-C surfactant, bLES and Infasurf still showed a dose response, so adding rSP-C to plain lipids was enough to match the natural extracts.
Early treatment in rats
Given about ten minutes after the last lavage at 25, 50 or 100 mg/kg, the rSP-C surfactant improved oxygen at two hours more than the identical lipid mixture without the protein, about as much as bLES and more than Alveofact. It also did the most to prevent hyaline membranes forming.
Grading the rat lavage model
Varying the number and volume of lung washes produced graded injury in rats. Doses of 12.5, 25 and 100 mg/kg of rSP-C surfactant improved oxygen and reduced hyaline membranes in proportion to dose at every severity, but did not change neutrophil influx or oedema. Antibody staining showed the drug spread evenly along the air-sac lining of washed lungs, but patchily around the larger airways in lungs that still had their own surfactant.
Dose finding in adult sheep
In adult sheep with saline-lavage lung injury, doses of 25, 100 and 200 mg lipid/kg of the recombinant SP-C surfactant all improved gas exchange; 100 and 200 mg/kg were better than 25 and equal to each other. Placing the drug into each lobe through a bronchoscope worked no better than pouring it down the breathing tube and took about twice as long (24.5 against 11.6 minutes).
No anaphylaxis in sensitised guinea pigs
Guinea pigs were sensitised to the rSP-C/phospholipid suspension and then challenged with it in the airway at up to 4 mg rSP-C with 200 mg lipid per kg. Every ovalbumin-sensitised control died within four minutes of challenge, while the rSP-C groups showed no bronchoconstriction; one animal died, probably from the anaesthetic. Lung weight rose with dose and a mild eosinophil infiltrate appeared. Staining found the drug in the air sacs, type II cells and macrophages.
Added dexamethasone in rats
Pretreatment with dexamethasone (10 mg/kg into the abdomen) did not raise oxygen on its own in lavaged rats but reduced neutrophils and hyaline membranes. It improved oxygenation at both doses of the rSP-C surfactant (25 and 100 mg/kg) and added histological benefit at the low dose, whereas it added nothing to oxygen or membranes with the protein-free Exosurf.
Lavaged pigs
Pigs with saline-lavage lung injury received the rSP-C surfactant, made of the protein with DPPC, phosphatidylglycerol and palmitic acid, at 50 or 100 mg/kg in volumes of 1 to 6 mL/kg. Four hours later the best group (50 mg/kg in 2 mL/kg) had a mean arterial oxygen of 332 Torr against 86 with phospholipid alone. The lipid spread evenly and hyaline membranes were fewer.
Combined with roflumilast in rats
In lavaged rats, the PDE-4 inhibitor roflumilast given into the airway at 6 mg/kg did not improve oxygen by itself but did prevent hyaline membranes and neutrophil influx. Both doses of the rSP-C surfactant (25 and 100 mg phospholipid/kg) raised oxygen, and adding roflumilast raised it further and cut hyaline membranes more than either treatment alone.
With C1 inhibitor in rats
Thirty-six lavaged rats received C1 esterase inhibitor (200 U/kg), r-SP-C surfactant (25 mg/kg) or both at 60 minutes. At 210 minutes arterial oxygen was 456 mm Hg with the surfactant and 387 with the combination, against 72 in controls and 63 to 120 with C1 inhibitor alone. The combination left fewer neutrophils in the air sacs than the surfactant alone.
Inflammation in ventilated premature lambs
Preterm lambs ventilated gently for six hours were treated with whole natural sheep surfactant, a lipid extract of it, Survanta or Venticute. The four could not be told apart on gas exchange, compliance or lung volume. Ventilation itself raised protein, inflammatory cells and inflammatory messengers compared with unventilated lambs, and none of the surfactants reduced these signs more than the others.
Meconium aspiration in piglets: inflammation
Newborn piglets given meconium into the lungs were treated 30 minutes later with a 75 mg/kg bolus of rSP-C surfactant or natural bovine surfactant, or left untreated. Both surfactants improved gas exchange and lung function. Lung histology scored better with rSP-C than in controls, the IL-1 beta signal was lower after rSP-C than after the bovine product or no treatment, and IL-10 rose in both treated groups.
With a COX inhibitor in rats
Adding the cyclooxygenase inhibitor eltenac, either into a vein or mixed into the surfactant, improved oxygen and hyaline membranes when combined with the low dose of rSP-C surfactant in lavaged rats, while eltenac alone did not raise oxygen. The best intratracheal mix carried about 0.3 mg/kg of eltenac. Confocal microscopy linked hyaline membranes to leaked fibrinogen, which eltenac reduced and surfactant alone did not.
Aspirated acidified infant formula in rabbits
Rabbits given acidified infant formula into the lungs were treated 30 minutes later with rSP-C surfactant at 0.5 or 2 mg SP-C/kg. At four hours arterial oxygen was 162 and 152 mm Hg with treatment against 61 without, compliance roughly two to three times higher, and the lung injury score fell from 14 to 7. The two doses worked equally well.
Meconium aspiration in piglets: lung genes
In the same piglet meconium model, a 75 mg/kg bolus of rSP-C surfactant or natural surfactant improved gas exchange, lung function and the fine structure of the lung seen by electron microscopy. Meconium had raised SP-B and lowered SP-C gene activity, and neither surfactant changed those gene or protein levels within the study's five and a half hours.
Premature rabbits: the role of PEEP
Preterm rabbits born three days early were given 100 mg/kg of rSP-C surfactant or bovine surfactant and ventilated for 30 minutes with or without positive end-expiratory pressure (PEEP). The rSP-C product depended on PEEP: dynamic compliance was 4.45 mL/kg with it and 2.58 without, while the bovine product gave 4.86 and 4.24 and saline 2.41 and 1.55.
Inhaled as a dry powder
A new dry-powder aerosolizer produced rSP-C surfactant particles with a median size of 1.6 micrometres (85% under 5) at about 800 mg per minute, without harming the material's function. Roughly 500 mg inhaled through the ventilator largely restored gas exchange and compliance in rabbits with lavage-and-ventilator injury and in rabbits four days after inhaled bleomycin, and restored compliance in bleomycin-injured mice breathing on their own.
Dosing Data
Lusupultide was never approved, so there is no label dose. The only per-dose amount stated in the abstracts read is the one below, used across the ARDS trials; it was given down a breathing tube by intensive care teams.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no regulator's label that says in what form Lusupultide is supplied. It is prepared and given by clinical staff, not bought and mixed at home: the next part says where.
Mixing a vial: a worked example
Nothing to mix at home, and no syringe units to work out: Lusupultide is prepared and given by clinical staff, in intensive care, for ventilated adults with lung injury.
In the carded trials it was instilled through the breathing tube into the lungs of ventilated adults with ARDS or severe pneumonia or aspiration.
Source: PMID 15329426 and PMID 21148720 (studies carded under Research below).
Storage before and after mixing
Unknown: no label on file says how Lusupultide is stored. It is kept and prepared by the hospital or clinic that gives it (see the part above); the home rules for a mixed vial in the mixing guide do not apply to it.
How it is taken
As it was given in human studies: Intratracheal, through the breathing tube (Up to 4 doses; Study: ARDS, pooled analysis of five trials).
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: a half-life of about 11 hours from rabbit lungs; 28 hours in mice. After about five half-lives almost none is left.
How long the doses were given: Study: ARDS, pooled analysis of five trials: Within 24 hours.
When effects appear: unknown; no source on this page gives a time to effect for Lusupultide. Results reported in the studies are under Published Research.
Source: half-life: PMID 9609732; Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: Instillation was well tolerated in the first North American trial (PMID 12649125); No difference in 28-day deaths or time on the ventilator between treated and untreated patients in any trial (PMIDs 15329426, 21148720); No anaphylactic reaction in guinea pigs sensitised and then challenged with it, though a mild eosinophil infiltrate and higher lung weight appeared (PMID 10661808); Briefly more dying eosinophils at one hour in the laboratory, not seen later (PMID 19295237). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Lusupultide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the trials and animal studies above”).
Interactions
Unknown: a PubMed search for human interaction studies of Lusupultide (reviewed 2026-11-03) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Lusupultide products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Lusupultide's expected mass, 3,618.7 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Not FDA Approved (Not approved: Drugs@FDA and the openFDA label endpoint return no record for lusupultide or Venticute (searched November 3, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the trials and animal studies above. The abstracts read report no new safety signal, but they give few details of adverse events.
Contraindications & Cautions
There is no label. These cautions follow from how it was tested.
Legal Status
Lusupultide is an investigational drug; no trial has been registered since its last phase 3 study ended in 2008. It is not approved in any jurisdiction checked.
Frequently Asked Questions
?What is lusupultide?
A recombinant copy of human surfactant protein C, one of the small proteins that help the lung's lining film work. It has 34 amino acids, three of them changed from the natural protein, and it was given mixed with lipids as the surfactant Venticute.
?What is Venticute?
The drug product: lusupultide mixed with dipalmitoylphosphatidylcholine, phosphatidylglycerol and palmitic acid, made into a suspension and instilled into the lungs through a breathing tube (PMID 10658037).
?Did it work for ARDS?
It improved blood oxygen during treatment in the early trials (PMIDs 15329426, 18689599), but no trial found that it reduced deaths or time on a ventilator, and the final trial of 843 patients found no benefit at all (PMID 21148720).
?Why did the last trial fail?
Oxygenation did not improve as it had before. The investigators found that a step added to the resuspension process for that trial appears to have partly inactivated the surfactant, so patients may have received a less active product (PMID 21148720).
?Is it the same as lucinactant (Surfaxin)?
No. Lucinactant is a different synthetic surfactant whose peptide, sinapultide, mimics surfactant protein B. Lusupultide is a recombinant form of surfactant protein C.
?Is lusupultide approved or available?
No. Drugs@FDA has no record of it, and ClinicalTrials.gov lists no study after the phase 3 trial that ended in 2008.
?How long does it stay in the lung?
In rabbits the lung cleared it with a half-life of about 11 hours, the same as native SP-C; in mice about 28 hours (PMID 9609732). No human figure has been published.
References
- [other] ChEMBL CHEMBL2218909 (LUSUPULTIDE; synonyms rSP-C surfactant, B-9420-001), protein sequence GIPFFPVHLKRLLIVVVVVVLIVVVIVGALLIGL, full molecular formula C182H310N40O35, molecular weight 3618.73; read November 3, 2026. https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL2218909/
- [other] US FDA, Drugs@FDA and drug label endpoints (openFDA), searched November 3, 2026: no record for lusupultide or Venticute. ClinicalTrials.gov, searched November 3, 2026: one study, NCT00074906 (Venticute, phase 3, Takeda, completed 2008). https://clinicaltrials.gov/study/NCT00074906
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- [pubmed] Hilgendorff A, et al. "Synthetic and natural surfactant differentially modulate inflammation after meconium aspiration." Intensive Care Med, 2003;29(12):2247-2254. PMID: 12955179.
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- [clinical-trial] Markart P, et al. "Patients with ARDS show improvement but not normalisation of alveolar surface activity with surfactant treatment: putative role of neutral lipids." Thorax, 2007;62(7):588-94. PMID: 17287298.
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- [pubmed] Erpenbeck VJ, et al. "Therapeutic surfactants modulate the viability of eosinophils and induce inflammatory mediator release." Int Arch Allergy Immunol, 2009;149(4):333-42. PMID: 19295237.
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Sources & Citations
Every study on this page was read from its PubMed record on November 3, 2026. The sequence and formula come from ChEMBL; status comes from Drugs@FDA (openFDA) and ClinicalTrials.gov, read the same day. Grey Peptides sells nothing and links to no vendor.
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