Solnatide
A 17-amino-acid ring copied from the tip of TNF, breathed in to help flooded lungs drain
Solnatide, also called AP301 or the TIP peptide, is a small ring of amino acids that reproduces one part of the inflammatory protein TNF: not the part that triggers inflammation, but a sugar-binding patch at the tip of the molecule. That patch switches on the epithelial sodium channel, the pump that pulls salt, and with it water, out of the air sacs. The idea behind the drug is that a lung filling with fluid can be helped to drain itself. It has been nebulised in healthy volunteers, in people on ventilators with acute respiratory distress syndrome, and in lung transplant recipients whose new lungs worked poorly in the first days. The larger placebo-controlled trials have not shown a clear benefit on their main measurements; a small transplant study and some subgroup analyses looked more promising. It holds orphan designation in Europe and the United States and is approved nowhere.
Used in human trials: 100 mg, Twice a day, Inhaled (nebulised) (Study: COVID-19 ARDS pilot trial) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
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What is it?
TNF has a bad reputation, earned by the receptor-binding faces that drive fever, inflammation and cell death. The protein also carries something else: a short loop at the tip of each subunit that binds particular sugars and has nothing to do with those receptors. Work through the 1990s and 2000s showed that this lectin-like domain helps the lung clear fluid. Solnatide is that loop made as a free-standing drug, a 17-amino-acid chain closed into a ring by a disulfide bond between its two cysteines. Because it sits at the tip of TNF, most papers simply call it the TIP peptide; its development code is AP301.
Its target is the epithelial sodium channel. In the lining of the air sacs, this channel takes sodium out of the thin film of liquid on the alveolar surface; water follows, and the gas-exchange surface stays thin enough to work. Patch-clamp experiments found that solnatide increases the amiloride-sensitive sodium current in alveolar cells from several species, and later studies pinned down how: it binds sugar groups on the outer loop of the channel's alpha subunit and a second site further in, which holds the channel open more of the time rather than putting more channels in the membrane.
The clinical target was pulmonary permeability oedema, the flooding seen in acute respiratory distress syndrome. ARDS has no drug treatment, only careful ventilation and support, and a drug that helped the lung drain itself would be new. Animal work in rats, mice, dogs and pigs reported less lung water and better oxygenation after inhalation, though not in every model: in pigs injured with oleic acid, where the alveolar lining dies rather than leaks, the benefit disappeared, and in mice with a severe pneumonia virus infection there was no effect at all.
In people, a first-in-man study nebulised single ascending doses in 48 healthy men and found no dose-limiting problems, with very little of the peptide reaching the blood. A phase 2a trial in 40 ventilated ARDS patients missed its main measurement, the change in extravascular lung water, with a signal only in a post-hoc subgroup of the sickest patients. A pilot study after lung transplantation reported better oxygenation and a shorter time on the ventilator in ten treated patients, which the authors were careful to call a proof-of-concept finding. A pilot trial in COVID-19 ARDS stopped early for slow recruitment and found no difference in ventilator-free days or survival. The phase 2b dose escalation trial finished enrolling 92 patients and completed in December 2024; its results have not been posted.
Beyond the lung, the same channel-opening action has been tried in other settings. Because solnatide can restore current through mutant channels that cause pseudohypoaldosteronism type 1B, a rare salt-wasting disease, it holds orphan designation for that condition in both Europe and the United States. Animal studies have reported anti-inflammatory effects in kidney and joint inflammation. None of this has produced an approved medicine, and every amount listed on this page comes from a published study.
Mechanism of Action
Solnatide copies the sugar-binding loop at the tip of TNF and uses it to hold the epithelial sodium channel open, which pulls salt and water out of flooded air sacs and steadies the cells lining the lung's capillaries.
Holds the sodium channel open
It binds sugar groups on the outer loop of the channel's alpha subunit and a second site where that subunit's tail meets the membrane, increasing the fraction of time the channel is open rather than adding channels (PMIDs 24077967, 26254591, 27645999).
Drains the air sacs
Sodium uptake through the channel is what pulls water off the alveolar surface, so the current it raises in alveolar cells from dog, pig and rat translates into faster clearance of oedema fluid in animal lungs and in perfused human lungs (PMIDs 23313096, 40485585).
Steadies the capillary barrier
Lung capillary endothelial cells carry the same channel subunit. Activating it limits oxidant production and the cytoskeletal signalling that pulls those cells apart during bacterial toxin exposure or spike-protein injury (PMIDs 28785264, 39405473, 37638055).
Avoids TNF's inflammatory faces
The loop it copies sits away from TNF's receptor-binding sites, so it does not trigger the inflammatory signalling that TNF blockers are used to suppress, and animal work reports anti-inflammatory effects in kidney and joint models (PMIDs 35264975, 30905471, 36389831).
Published Research
The studies below were read from their PubMed abstracts in November 2026: the human trials in healthy volunteers, ARDS, COVID-19 ARDS and lung transplantation; animal work in rats, mice and pigs; the cell experiments that identified the sodium channel as its target; and two reviews. Many papers title the drug by the TNF domain it copies rather than by its name, so those cards carry a sweep record quoting the abstract phrase that names the peptide. Studies of its congener AP318 and of other synthetic variants are listed under References, because they tested different molecules.
First study in people: single inhaled doses
Forty-eight healthy men were randomised in six ascending dose groups, up to a single 120 mg inhalation, three on drug for each on placebo. Everyone completed the protocol. There were no serious, local or dose-limiting adverse events, and spirometry, exhaled nitric oxide, vital signs, ECG and laboratory tests showed no pattern by dose or time. Peak blood levels stayed below 2.5 ng/mL even in the highest groups, which the authors read as the drug staying largely in the lung.
Phase 2a in ARDS: no change in lung water
Forty ventilated adults with ARDS were randomised to inhaled drug or saline twice daily for seven days. The main measurement, baseline-adjusted change in extravascular lung water index by thermodilution, did not differ between groups (p = 0.196), and neither did oxygenation, ventilation pressures, lung injury score or 28-day mortality. Inhalation was well tolerated. A post-hoc subgroup of patients with a baseline SOFA score of 11 or more showed less lung water and lower ventilation pressures, which the authors presented as a hypothesis for later trials.
Pilot study after lung transplantation
Twenty recipients who developed primary graft dysfunction after a first lung transplant were randomised one to one to nebulised drug or placebo twice daily for up to seven days. Oxygenation improved more in the treated group by 72 hours (p = 0.049), and intubation was shorter, about two days against nearly four (p = 0.02). Intensive care stay trended shorter without reaching significance, everyone survived 30 days, and no severe adverse events were recorded. The authors stress that a 20-patient pilot was not powered for firm conclusions.
COVID-19 ARDS: no difference, stopped early
At two centres in Vienna, mechanically ventilated adults with moderate to severe COVID-19 ARDS were randomised to inhale 100 mg or placebo twice daily for seven days. Thirty of a planned 40 patients were enrolled before slow recruitment ended the trial. Ventilator-free days within 28 days were zero in both groups, and survival at 28 days was 11 of 15 on drug against 9 of 15 on placebo. Adverse events were counted in both arms and none was judged related to the study treatment.
The phase 2b trial protocol
The published protocol for the phase 2b study: ventilated patients with moderate to severe ARDS and permeability oedema randomised to ascending doses or placebo, dosed twice daily for seven days and followed for a further 21 days, with a data safety monitoring board reviewing each step before a higher dose group opened. The authors discuss the practical difficulty of consent, since eligible patients are usually sedated or comatose when the short enrolment window opens.
Interim look during the pandemic
An ad hoc interim analysis of the first 16 patients in the phase 2b trial, five with COVID-19 ARDS and eleven with ARDS from other causes, done so the monitoring board could decide whether to keep enrolling during the pandemic. The COVID-19 patients were less severely ill at entry and survived more often, while oedema and ventilation measurements did not differ by cause. The board found no sign of added risk or of distorted study data and allowed the trial to continue.
Measuring the peptide in blood
A chromatography and mass spectrometry method, validated with a carbon-13 labelled internal standard, that detects 1 ng of the peptide per millilitre of human plasma from a 50 microlitre sample. Precision ran between about 6 and 10 percent and accuracy between 96 and 100 percent across three batches, and the peptide survived three freeze-thaw cycles and twenty weeks frozen. This was the assay used to measure blood levels after inhalation in the phase 1 study, and the paper gives the molecular weight as 1923.1 with the ring closed by a disulfide bond.
High-altitude lung oedema (rats)
Rats were exercised to exhaustion in a chamber simulating 4,500 metres, then held at 6,000 metres for 48 hours, a model of high-altitude pulmonary oedema. Three doses of the peptide were compared with saline, dexamethasone, aminophylline and two inflammation inhibitors over three days. Treated animals had less protein in lavage fluid and less lung water, less bleeding and better preserved alveolar-capillary structure, and more of the tight-junction protein occludin than high-altitude controls or the dexamethasone and aminophylline groups.
Inhaled in injured pig lungs
Lung injury was produced in 16 pigs by washing out surfactant and then ventilating them harmfully. Animals were randomised to nebulised peptide at 1 mg/kg or to water for injection and watched for five hours. Lung water fell and the oxygenation ratio rose in the treated group, with no change in controls, and the shunt fraction also favoured treatment. This was the model that supported moving the inhaled peptide into patients.
A model where it did not work (pigs)
The same group repeated its protocol in six pigs injured by injecting oleic acid, which kills alveolar lining cells rather than simply making them leak, and compared the results with the lavage-injury experiments. Ventilation-perfusion matching improved only in the lavage model. Gas exchange and oedema did not respond after oleic acid. The authors concluded that a drug working through the alveolar epithelium should not be expected to help when that epithelium is destroyed.
Severe viral pneumonia (mice)
Mice infected with pneumonia virus of mice, a model of severe respiratory syncytial virus disease, were given the peptide or saline into the trachea on day five or day seven after infection, and in a separate experiment repeatedly. Lung wet-to-dry weight ratios were unchanged at every time point and dose schedule, as were clinical severity scores and the cells recovered from the lungs. The authors report a plain negative result in this infection.
Rat lung transplantation
The peptide was instilled into the donor lung immediately before single-lung transplantation in rats. Oxygenation 24 hours later was better than with an inactive mutant peptide, and fewer neutrophils appeared in lavage fluid. Both effects were abolished by amiloride, which blocks the sodium channel, pointing to the channel as the route of benefit. Reactive oxygen species fell in transplanted lungs and in endothelial cells put through hypoxia and reoxygenation.
Antibody-driven kidney inflammation (mice)
In nephrotoxic serum nephritis, a mouse model of antibody-mediated glomerulonephritis, injection into the abdomen reduced inflammation, protein in the urine and blood urea nitrogen, and delivery aimed at the glomerulus improved kidney pathology and cut mortality in the severe form. The protective effect was blocked by indomethacin, implicating prostaglandins, and the peptide activated the sodium channel on glomerular endothelial cells without raising blood pressure.
Joint inflammation (mice)
In antigen-induced arthritis the peptide reduced the influx of cells into the joint and the release of inflammatory mediators, with less swelling and less tissue damage than controls. The authors frame the result as evidence that TNF's lectin-like domain is anti-inflammatory in the joint even though the rest of the protein drives joint destruction, and that copying only this domain avoids the infection risk of blocking TNF altogether.
Pneumococcal capillary leak (mice and cells)
Mice lacking the sodium channel's alpha subunit in their lung endothelium leaked more after pneumococci or the toxin pneumolysin were instilled into the airway, and their lung endothelium showed more of the superoxide-generating enzyme NOX2. Treating infected normal mice with the peptide reduced capillary leak without measurably increasing bacterial load in the lung, and in human lung endothelial monolayers it blocked toxin-induced leak much as a NOX2 inhibitor did.
Spike protein vasculopathy (mice and cells)
The receptor-binding part of the SARS-CoV-2 spike protein impaired sodium channel activity in human lung endothelial cells, lowered surface ACE2, and raised reactive oxygen species and tissue factor, weakening the barrier. The peptide reversed those changes in culture. In mice engineered to carry human ACE2, pretreatment with the spike fragment worsened fibrin deposition and leak after pneumococcal infection, and treatment with the peptide reduced both.
Donated human lungs perfused outside the body
Human lungs that could not be transplanted were perfused in the laboratory and infected with Streptococcus pneumoniae, then treated with the peptide. Protein leak across the barrier and oedema formation fell, clearance of fluid from the air sacs rose, and the inflammatory signals interleukin-6 and interleukin-8 dropped in the airspaces. Fewer bacteria crossed into the perfusate. The authors present this as three distinct mechanisms of benefit measured in human lung tissue.
The sodium channel is the target
Patch-clamp work in a lung cell line and in kidney and ovary cells engineered to carry human channel subunits showed that the peptide acts on the epithelial sodium channel itself. It increased current through channels that had already been cleaved into their active form but not through near-silent uncleaved ones, needed either the alpha or the delta pore-forming subunit together with beta and gamma, and lost its effect when sugar groups were stripped from the channel's outer loops.
Alveolar cells from three species
In whole-cell recordings from type II alveolar cells freshly isolated from dog, pig and rat lungs, the amiloride-sensitive sodium current rose roughly ten to sixteen-fold when the peptide was added. In a human lung cell line the increase vanished when sodium was replaced in the bath or when the channel was blocked beforehand, but was unaffected by blockers of cyclic-nucleotide-gated channels, which points to the epithelial sodium channel as the conduit.
Sugar groups are needed
Mutating the sites where sugars attach to the channel's alpha or delta subunit, alone and in combination, and separately truncating the alpha subunit's tail, showed that both features matter. Activation was weakened by removing either one and abolished when both were removed together. The authors describe an interaction that depends on the channel's sugar chains and that restores sodium and fluid uptake in flooded air sacs toward normal.
A second binding site inside the channel
Docking calculations suggested three residues where the channel's second membrane-spanning region meets its tail. Replacing two or three of them with alanine cut binding of both the peptide and TNF and abolished the increase in the fraction of time the channel stayed open, while the mutant channels still assembled and worked normally. The peptide's separate effect of reducing channel tagging for degradation was unaffected, so the two actions are distinct.
Protecting the channel during bacterial injury
Combining biochemistry, electrophysiology and mice carrying a mutant TNF, this study found that the peptide activates the sodium channel directly, not the basolateral sodium pump, by binding the alpha subunit's tail. In the presence of the pneumococcal toxin pneumolysin it stabilised the complex that keeps the channel open and preserved the alpha subunit by damping a protein kinase C pathway. Mice whose own TNF lacked this activity flooded more easily after low-dose toxin.
Barrier function in lung capillary cells
Human lung microvascular endothelial cells turned out to carry all three channel subunits plus a related acid-sensing channel. The peptide, and separately a direct activator of that related channel, strengthened the barrier of monolayers damaged by pneumolysin. Depleting the alpha subunit made cells more vulnerable and blunted both drugs, and the peptide reduced phosphorylation of a kinase and of the actin-binding protein filamin A, which links it to the cytoskeleton.
Channel mutants that cause a salt-wasting disease
Ten frameshift mutations in the channel's alpha subunit reported in pseudohypoaldosteronism type 1B were expressed in cells; all carried less current than normal channels. The peptide restored current to normal levels or above, even though these mutants lack the internal site it binds, so activation of the beta and gamma subunits may contribute. TNF itself behaved similarly, supporting the view that the peptide reproduces the cytokine's lectin-like action.
More disease mutants restored
A companion study tested point mutations at conserved positions that cause the same disease. Every mutant channel carried less sodium current than normal, and the amount of channel protein reaching the membrane varied widely between them. Both this peptide and the congener AP318 raised current to the level of normal channels or higher. Since treatment for the disease is only supportive, the authors propose direct channel activation as a drug strategy.
Listeria toxin and endothelial leak
Listeriolysin, the main toxin of Listeria monocytogenes, made monolayers of human lung microvascular endothelial cells leak in proportion to dose, alongside more reactive oxygen species and contractile signalling. A protein kinase C inhibitor prevented the leak entirely. The peptide blunted it too, by damping that kinase, reducing oxidant production and restoring the balance between two regulators of the cell skeleton.
What the ring looks like in solution
Nuclear magnetic resonance showed that the peptide does not hold one rigid shape but moves through a set of related conformations with a small greasy core and two electrically charged ends. Using that picture and the published channel structure, the authors propose a model of how it docks onto the tail of the channel's alpha subunit, meant as a starting point for testing the interaction and for designing analogues.
Review: TNF's two faces in the lung
A review of how the same cytokine can both injure and protect the lung. Signalling through one TNF receptor drives inflammation and impairs barrier function and fluid clearance, while the lectin-like domain, reproduced by this 17-residue peptide, supports the barrier and increases clearance in both hydrostatic and permeability oedema models. It notes that the domain stays active when TNF is bound to its soluble receptors, and that it does not interfere with TNF's antibacterial role.
Review: the sodium channel as a drug target
A survey of drugs aimed at the epithelial sodium channel, where gain and loss of function cause conditions from Liddle syndrome to generalised pseudohypoaldosteronism. The review notes that many candidate compounds look better in cells and animals than in patients, and lists this peptide, holding orphan designation from both the European and US regulators, as the channel activator then in phase 2 testing in acute respiratory distress syndrome.
Dosing Data
Every amount below was given inside a clinical trial, nebulised and breathed in. There is no approved product and no approved dose, and the trials that used these amounts largely did not show benefit on their main measurements.
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 label and no published test that says what forms or vial sizes Solnatide is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
No worked example: none of the doses on this page is a fixed amount in mg or mcg injected under the skin or into a muscle (the routes given are: inhaled (nebulised)). There is no home-mixing step to show. The reconstitution calculator does the arithmetic for any vial.
Source: the route and amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Solnatide, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Solnatide stays intact once mixed.
How it is taken
As it was given in human studies: Inhaled (nebulised) (Twice a day; Study: COVID-19 ARDS pilot trial).
For injection technique, sites and needle disposal, see the mixing guide.
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 not reported in the sources read. After about five half-lives almost none is left.
How long the doses were given: Study: COVID-19 ARDS pilot trial: 7 days; Study: first-in-man single doses in healthy men: Single dose.
When effects appear: unknown; no source on this page gives a time to effect for Solnatide. Results reported in the studies are under Published Research.
Source: half-life: PMID 24515273; 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: No serious, local or dose-limiting adverse events in 48 healthy men given single inhaled doses, including no hoarseness, cough or bronchospasm (PMID 24515273); Inhalation described as well tolerated in the 40-patient phase 2a ARDS trial, with no difference in 28-day mortality (PMID 28750677); No severe adverse events and 100% survival at 30 days in the 20-patient lung transplant pilot (PMID 29055604); In the COVID-19 ARDS pilot, adverse and serious adverse events occurred in both arms and none was judged related to the study drug (PMID 40280364); Very little of the peptide reaches the bloodstream after inhalation, with peak levels under 2.5 ng/mL at the highest doses tested (PMID 24515273). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Solnatide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the trials above”).
Interactions
Unknown: a PubMed search for human interaction studies of Solnatide (reviewed 2026-11-04) 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 Solnatide 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 Solnatide's expected mass, 1,923.1 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: In Clinical Trials (Not approved anywhere). 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 above. They were small, and most participants were critically ill, which makes adverse events hard to attribute.
Contraindications & Cautions
There is no label, so there are no official contraindications. These cautions follow from how and where it has been studied.
Legal Status
Solnatide is an investigational drug with orphan designation on both sides of the Atlantic and no marketing approval anywhere.
Frequently Asked Questions
?What is solnatide?
A ring of 17 amino acids that reproduces the sugar-binding loop at the tip of the TNF protein. It is breathed in as a mist and switches on the epithelial sodium channel, the pump that drains fluid from the air sacs of the lung. It is also called AP301 or the TIP peptide.
?Is it the same as a TNF blocker?
No, close to the opposite. TNF blockers such as the arthritis biologics stop the cytokine reaching its receptors. Solnatide copies a different part of the same protein, one that has nothing to do with those receptors, so it does not suppress TNF's role in fighting infection.
?Did it work in ARDS?
Not on the measurements the trials were built around. The phase 2a trial found no difference in lung water, and a COVID-19 ARDS pilot found no difference in ventilator-free days or survival. A subgroup of the sickest patients in the phase 2a trial looked better, which is a hypothesis rather than a result. The larger phase 2b trial completed in December 2024 and has posted nothing.
?What was the lung transplant study?
A 20-patient pilot in recipients whose transplanted lungs worked poorly in the first hours. Those given the drug had better oxygenation by three days and came off the ventilator sooner. With ten patients per group the authors called it proof of concept, not proof of benefit.
?Why does it have orphan designation?
Because of two rare conditions: poor function of a newly transplanted lung, and pseudohypoaldosteronism type 1B, a salt-wasting disease caused by faulty sodium channels that the peptide can switch back on in cell experiments. Designation is a regulatory incentive for rare-disease development, not an approval.
?Can I buy it?
No. It has never been approved or marketed anywhere and has only been supplied inside clinical trials, usually to patients on ventilators in intensive care.
References
- [clinical-trial] Schwameis R, et al. "A FIM study to assess safety and exposure of inhaled single doses of AP301-A specific ENaC channel activator for the treatment of acute lung injury." J Clin Pharmacol, 2014;54(3):341-50. PMID: 24515273.
- [clinical-trial] Krenn K, et al. "Inhaled AP301 for treatment of pulmonary edema in mechanically ventilated patients with acute respiratory distress syndrome: a phase IIa randomized placebo-controlled trial." Crit Care, 2017;21(1):194. PMID: 28750677.
- [clinical-trial] Aigner C, et al. "Treatment of primary graft dysfunction after lung transplantation with orally inhaled AP301: A prospective, randomized pilot study." J Heart Lung Transplant, 2017. PMID: 29055604.
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- [clinical-trial] Schmid B, et al. "Safety and preliminary efficacy of sequential multiple ascending doses of solnatide to treat pulmonary permeability edema in patients with moderate-to-severe ARDS-a randomized, placebo-controlled, double-blind trial." Trials, 2021;22(1):643. PMID: 34544463.
- [clinical-trial] Schmid B, et al. "Safety and preliminary efficacy of sequential multiple ascending doses of solnatide to treat pulmonary permeability edema in patients with moderate to severe ARDS in a randomized, placebo-controlled, double-blind trial: preliminary evaluation of safety and feasibility in light of the COVID-19 pandemic." Trials, 2022;23(1):252. PMID: 35379296.
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- [pubmed] Czikora I, et al. "Epithelial Sodium Channel-α Mediates the Protective Effect of the TNF-Derived TIP Peptide in Pneumolysin-Induced Endothelial Barrier Dysfunction." Front Immunol, 2017;8:842. PMID: 28785264.
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- [pubmed] Willam A, et al. "Restoration of Epithelial Sodium Channel Function by Synthetic Peptides in Pseudohypoaldosteronism Type 1B Mutants." Front Pharmacol, 2017;8:85. PMID: 28286482.
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- [pubmed] Martin-Malpartida P, et al. "Conformational ensemble of the TNF-derived peptide solnatide in solution." Comput Struct Biotechnol J, 2022;20:2082-2090. PMID: 35601958.
- [review] Lucas R, et al. "Dichotomous Role of Tumor Necrosis Factor in Pulmonary Barrier Function and Alveolar Fluid Clearance." Front Physiol, 2021;12:793251. PMID: 35264975.
- [review] Lemmens-Gruber R, et al. "The Epithelial Sodium Channel-An Underestimated Drug Target." Int J Mol Sci, 2023;24(9). PMID: 37175488.
- [pubmed] Hartmann EK, et al. "Inhalation therapy with the synthetic TIP-like peptide AP318 attenuates pulmonary inflammation in a porcine sepsis model." BMC Pulm Med, 2015;15:7. PMID: 25879802.
- [pubmed] Hartmann EK, et al. "TIP peptide inhalation in experimental acute lung injury: effect of repetitive dosage and different synthetic variants." BMC Anesthesiol, 2014;14:42. PMID: 24904234.
- [pubmed] Hazemi P, et al. "Essential structural features of TNF-α lectin-like domain derived peptides for activation of amiloride-sensitive sodium current in A549 cells." J Med Chem, 2010;53(22):8021-9. PMID: 20979368.
- [pubmed] Marquardt A, et al. "Identification, affinity characterisation and biological interactions of lectin-like peptide-carbohydrate complexes derived from human TNF-alpha using high-resolution mass spectrometry." J Pept Sci, 2007;13(12):803-10. PMID: 17918767.
- [pubmed] Zhuang B, et al. "Tolerability, safety and efficacy of a novel phosphate binder VS-505 (AP301): a Phase 2 dose-escalation and dose-ranging study in patients undergoing maintenance hemodialysis." Nephrol Dial Transplant, 2024;39(10):1649-1661. PMID: 38453435.
- [pubmed] Ware LB. "Targeting resolution of pulmonary edema in primary graft dysfunction after lung transplantation: Is inhaled AP301 the answer?." J Heart Lung Transplant, 2017. PMID: 29198870.
- [pubmed] Eaton DC, et al. "Endothelial ENaC as a repressor of oxidative stress and a guardian of lung capillary barrier function in bacterial and viral pneumonia." Front Physiol, 2025;16:1562626. PMID: 40260205.
- [registry] ClinicalTrials.gov API v2, read November 4, 2026: NCT01627613 (phase 2a, inhaled AP301 twice daily for 7 days against saline in 40 ventilated patients with acute lung injury, Medical University of Vienna, completed 2014, no results posted); NCT02095626 (pilot, inhaled AP-301 after lung transplantation, 20 patients, completed 2015); NCT03567577 (phase 2b, 'Solnatide 25 mg powder for reconstitution for solution for inhalation' against 0.9% saline in moderate-to-severe ARDS, 92 enrolled across 15 centres in Austria and Germany, completed December 27, 2024, no results posted). https://clinicaltrials.gov/study/NCT03567577
- [other] European Medicines Agency, orphan designation register, read November 4, 2026: EU/3/15/1549, designated October 9, 2015 for treatment of primary graft dysfunction following lung transplantation, and EU/3/15/1591, designated December 14, 2015 for treatment of pseudohypoaldosteronism type 1B; sponsor APEPTICO Forschung und Entwicklung GmbH, Austria. https://www.ema.europa.eu/en/medicines/human/orphan-designations/eu-3-15-1549
- [other] US FDA, Office of Orphan Products Development, Orphan Drug Designations and Approvals database, read November 4, 2026: solnatide designated February 8, 2016 for treatment of generalized systemic pseudohypoaldosteronism type 1 (also known as autosomal recessive PHA-I or PHA-IB); status designated, not approved for the orphan indication; sponsor APEPTICO Forschung und Entwicklung GmbH.
- [other] PubChem CID 91864495 ('Solnatide'; synonyms AP301, AP-301, TIP-peptide, CAS 259206-53-6): Cys-Gly-Gln-Arg-Glu-Thr-Pro-Glu-Gly-Ala-Glu-Ala-Lys-Pro-Trp-Tyr-Cys, cyclic (1->17) disulfide; molecular formula C82H119N23O27S2, molecular weight 1923.1. Read November 4, 2026. https://pubchem.ncbi.nlm.nih.gov/compound/91864495
- [other] US FDA, Drugs@FDA (openFDA drugsfda endpoint), searched November 4, 2026: no application for solnatide or AP301.
Sources & Citations
Every study on this page was read from its PubMed record on November 4, 2026. Trial registrations come from ClinicalTrials.gov, the structure and formula from PubChem, and regulatory status from Drugs@FDA, the EMA orphan register and FDA's orphan designations database, read the same day. Grey Peptides sells nothing and links to no vendor.
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