If you are 1 of the 1,255 people in ALOFT-IPF, you have spent at least a year taking a study drug twice a day, without knowing whether it is admilparant or a placebo, to help answer a question that matters to everyone with IPF. Admilparant works on a different scarring pathway than the 3 approved IPF drugs, and in Phase 2 the 60 mg dose slowed the loss of lung capacity, most clearly in people with progressive pulmonary fibrosis (Corte et al., AJRCCM, 2025). ClinicalTrials.gov estimated that the main IPF trial would finish collecting its key data on October 6th, 2 days before this post, though BMS last updated that record in March and has not said the date was met (NCT06003426). BMS has told reporters to expect results by the end of 2026.
On September 30th, a trade publication reported that Bristol Myers Squibb had added closer liver monitoring to the plan for the trials' follow-on study, after a limited number of liver events in the program. That news lands on a drug whose history runs through the liver. BMS's first drug of this kind damaged the liver and gallbladder in a trial reported in 2018. Its chemists then built admilparant by reworking that drug's structure, and the company's scientists later published why they believed the new drug would not cause the same harm.
What Bristol Myers Disclosed About Admilparant Liver Safety
The source is a protocol amendment, the formal change request a sponsor files when it alters how a trial runs. According to BioPharma Dive, BMS submitted it for European Union sites in May for the long-term safety extension of the ALOFT program, the follow-on study people move into after the main trials. The amendment listed liver injury as a "newly classified important potential risk" and required closer monitoring of anyone whose liver enzymes ran high, to decide whether they should stop the drug (BioPharma Dive, September 30, 2026).
The same document described most of the liver events as "mild, transient, or demonstrated patterns consistent with hepatic adaptation," a term this post returns to below. One participant died of multi-organ failure that included liver damage, destruction of red blood cells and widespread clotting, and that person had underlying lung disease and other complications. BMO Capital Markets analysts told BioSpace that a separate committee has been set up to look specifically at possible liver injury (BioSpace, October 1, 2026).
“Most events were mild, transient, associated with other medical conditions, and occurred in patients receiving concomitant medications known to cause elevations of liver enzymes. Most events resolved with no change to study treatment.”
Bristol Myers Squibb spokesperson, to Fierce Biotech, October 1, 2026
Two details shape how much weight the news can bear. The trial is still blinded, so the death and the liver events cannot yet be assigned to admilparant or to placebo. Analysts at Leerink, writing for investors, said the fatal case "did not demonstrate a classic drug-induced liver injury pattern" (Fierce Biotech, October 1, 2026). That is an outside reading of a document, not a finding from the trial, and the only thing that will settle it is the unblinded data.
BMS-986020, the LPA1 Drug That Came Before Admilparant
Admilparant blocks a receptor called LPA1, which responds to a fat-based signaling molecule involved in lung scarring. BMS tried this idea once before, with a drug called BMS-986020. In a Phase 2 trial of 143 people with IPF, the 600 mg twice-daily dose slowed the loss of lung capacity over 26 weeks compared with placebo, meeting the trial's main goal for that dose (Palmer et al., CHEST, 2018).
It also raised liver enzymes in a dose-related pattern, and the trial was stopped early after 3 people developed cholecystitis, inflammation of the gallbladder, that was judged to be caused by the drug once the treatment groups were unblinded (Palmer et al., CHEST, 2018). BMS ended development.
The 2026 news coverage we read skipped what came next. BMS chemists built admilparant by reworking BMS-986020's structure (Cheng et al., Journal of Medicinal Chemistry, 2021), and BMS toxicologists went looking for the cause of the liver damage, publishing it in 2022. BMS-986020 jammed the pumps liver cells use to push bile acids out, the digestive salts the liver makes and sends to the gallbladder, and it also interfered with mitochondria, the parts of a cell that make energy. When bile acids back up inside liver cells, the cells are damaged (Gill et al., Toxicology and Applied Pharmacology, 2022).
Gill et al., Toxicology and Applied Pharmacology, March 2022, a study by Bristol Myers Squibb scientists. A third pump, MRP3, is left off because BMS-986020 was weak against it too (22 micromolar). The paper did not test admilparant's effect on mitochondria.
The 2022 paper concluded that the earlier drug's liver toxicity "was unrelated to LPA1 antagonism," meaning it came from that particular molecule rather than from blocking the receptor, and it pointed to "the lack of hepatobiliary toxicity in nonclinical and clinical safety studies with BMS-986278," the code name for admilparant (Gill et al., 2022). Admilparant's Phase 2 results, posted on ClinicalTrials.gov, did not contradict it.
Those numbers are small, and a 26-week trial of 403 people cannot rule out a rare liver problem that only shows up in Phase 3 trials enrolling about 2,300 people for a year or longer. That gap between Phase 2 and Phase 3 is exactly where the 2026 liver reports sit.
The other well-known LPA1 failure has nothing to do with the liver, despite being mentioned in the same breath. Amgen's fipaxalparant, inherited from Horizon Therapeutics, was stopped in IPF in 2024 because its 153-person Phase 2 trial missed its primary goal and its key secondary goals (ClinicalTrials.gov, NCT05032066). That was an efficacy failure, not a safety one.
Hepatic Adaptation and the Admilparant Liver Events
When BMS describes events as "consistent with hepatic adaptation," it is using a concept the FDA lays out in its guidance on drug-induced liver injury. Liver enzymes such as ALT and AST leak into the blood when liver cells are stressed, and many drugs nudge them up for a while before they settle back down, even while the person keeps taking the drug.
“For most people, the liver appears capable of adapting to injury by foreign chemical substances, which may render a person tolerant to the drug despite continued exposure.”
FDA, Drug-Induced Liver Injury: Premarketing Clinical Evaluation, July 2009
The same guidance carries the caveat that matters here. It says "normalization of abnormalities on continued treatment is not proof that the abnormality was not drug-caused," because a liver that adapts was still reacting to the drug. Adaptation is reassuring about the person in front of you but says less about whether a drug, given to thousands of people, will occasionally cause serious harm.
For that, the FDA relies on a rule of thumb called Hy's Law, named for the liver specialist Hyman Zimmerman. The warning sign is a person whose ALT or AST rises to 3 times the upper limit of normal or more, whose bilirubin, a yellow waste product the liver clears, rises above 2 times its upper limit, and who has no other explanation such as viral hepatitis or a blocked bile duct. The guidance says drugs that produce such cases tend to cause severe liver injury at roughly a tenth of their rate, and that those cases appear against a background of more 3-fold enzyme rises on the drug than on the comparison treatment (FDA, 2009).
- 1xTop of normal. Each lab sets its own upper limit, so trial rules are written as multiples of it rather than as fixed numbers.
- 1.5xMost common entry cutoff in IPF trials. Of the 13 open IPF drug trials that print an ALT or AST cutoff, 6 turn people away above 1.5 times normal, the most common limit (Trial Friend analysis of ClinicalTrials.gov, October 8, 2026).
- 3xThe level FDA counts. A higher rate of 3-fold rises on the drug than on placebo is the sensitive early signal. With bilirubin above 2 times normal and no other cause, it becomes a Hy's Law case, the most specific warning.
- 5xConsider stopping if it lasts. FDA guidance suggests considering stopping a trial drug when ALT or AST stays above 5 times normal for more than 2 weeks.
- 8xConsider stopping. Above 8 times normal, FDA guidance suggests considering stopping the trial drug outright, whatever the symptoms.
Thresholds from FDA, Drug-Induced Liver Injury: Premarketing Clinical Evaluation, July 2009. The guidance also suggests stopping at 3 times normal when it comes with fatigue, nausea, vomiting, right upper abdominal pain, fever, rash or high eosinophils.
Read against that scale, "mild, transient" events and a single death with several possible causes are not the same kind of information. The first describes enzyme rises that came and went. The second is a case the trial's own records will have to classify, and nothing public yet says whether it met the Hy's Law pattern.
What the ALOFT-IPF Results Could Show About Admilparant
ALOFT-IPF compares 60 mg and 120 mg of admilparant twice a day against placebo for at least 52 weeks, with or without the approved drugs nintedanib or pirfenidone in the background (Maher et al., ATS 2025 abstract). Its main measure is how many milliliters of forced vital capacity, the amount of air a person can blow out, each group loses over a year. The 120 mg dose is twice the best dose in Phase 2, which is one more reason the liver numbers by dose will matter.
The reason so many people with pulmonary fibrosis are watching is what Phase 2 showed. Over 26 weeks, lung capacity measured as percent predicted FVC fell 1.1 points on 60 mg against 4.3 on placebo in progressive pulmonary fibrosis, and 1.2 against 2.7 in IPF, where the gap was smaller and less certain. The benefit appeared with or without nintedanib or pirfenidone, so admilparant could be added to the drugs people already take rather than replace them, and in the progressive pulmonary fibrosis group no one on 60 mg stopped treatment because of side effects, against 17.1% on placebo (Corte et al., AJRCCM, 2025). A later analysis, not planned in advance, found the 60 mg dose delayed disease progression in both groups, with a 46% lower risk of worsening over 26 weeks in IPF and a 59% lower risk in progressive pulmonary fibrosis (Kreuter et al., CHEST, 2025).
- Slows lung decline, liver numbers match placeboWhat it would meanThe cleanest case for a new kind of IPF pill, and for the LPA1 class, including Contineum's rival drug PIPE-791.What to look forRates of ALT or AST above 3 times normal similar on admilparant and placebo, and no Hy's Law cases on the drug.
- Slows lung decline, more liver rises on the drugWhat it would meanThe benefit would be weighed against a liver risk needing regular liver blood tests, which the labels for nintedanib and pirfenidone already require.What to look forMore 3-fold enzyme rises at 120 mg than at 60 mg or placebo, and how many people stopped treatment because of them.
- Misses its lung function goalWhat it would meanThe liver question would matter less for admilparant. Stifel analysts told investors the ALOFT-IPF outcome is core to the case for Contineum's rival LPA1 drug, PIPE-791.What to look forThe difference in milliliters of lung capacity lost over a year between each dose and placebo.
Outcomes framed by the trial's registered primary measure (ClinicalTrials.gov, NCT06003426) and the FDA's 2009 liver injury guidance. Topline announcements are short, and detailed safety tables usually come later at a medical meeting or in a journal.
The Admilparant Long-Term Extension and What ALOFT Participants Can Ask
The amended plan belongs to a study most people in ALOFT have not started yet. The long-term extension, listed on ClinicalTrials.gov as NCT07441408, is estimated to begin on December 16th and would give admilparant to about 2,380 people who complete either ALOFT trial, in a study planned to run about 3 years. Its main measures are all safety measures, including clinically significant lab abnormalities, and the European approval of the study, granted on June 21, 2026, covers 86 sites in 14 countries (CTIS, EU trial 2025-522373-10-00).
One rule in the listing deserves attention. Anyone whose study drug was stopped for good because of a side effect in ALOFT-IPF or ALOFT-PPF cannot join the extension. ClinicalTrials.gov currently shows 3 US sites for it, in Alabama, Florida and Pennsylvania, against 70 US sites in ALOFT-IPF, though sites are often added as a study starts.
- Which liver tests have I had, and how often?
- Trials check ALT, AST and bilirubin on a schedule. Ask whether your monitoring has changed in 2026, since BMS added closer liver monitoring for people with high enzymes.
- Have any of my results been above normal?
- A mild rise that settles is common with many drugs. Knowing your own numbers makes the published results easier to read against your experience.
- Will I be able to join the extension, and where?
- Ask whether your site plans to run the extension, which US sites are confirmed, and what happens if treatment was paused rather than stopped for good.
- Which of my other medicines can raise liver enzymes?
- BMS said most events happened in people also taking medicines known to raise liver enzymes. A pharmacist can go through your list.
- When will I learn which pill I was taking?
- Unblinding for participants usually comes after the full study ends. ALOFT-IPF's study completion date is estimated for June 4, 2027.
Other IPF Treatments and IPF Clinical Trials Open Now
People with IPF are not waiting on admilparant alone. The FDA has approved 3 drugs that slow the loss of lung function: pirfenidone, nintedanib and nerandomilast, sold as Jascayd, which the FDA approved for IPF on October 7, 2025, the first new IPF drug in more than a decade. The FDA's decision on inhaled treprostinil (Tyvaso) for IPF is expected in late April 2027.
Both ALOFT trials have stopped enrolling, so we looked at what else is open. On October 8th, ClinicalTrials.gov listed 106 recruiting or not-yet-recruiting studies whose own condition list names IPF, and 55 of them test a drug or biologic. Liver rules are a quiet filter across them.
Of the 13 trials that print an ALT or AST cutoff, 6 set it at 1.5 times normal, 3 at 2 times, 1 at 2.5 times, 2 at 3 times and 1 at 5 times.
That matters for anyone whose liver tests run a little high from another medicine or from fatty liver, which can rule them out of a trial before lung function is even measured. Only 20 of the 55 drug trials list a US site.
Contineum's PIPE-791, the other LPA1 drug in IPF, is in a 324-person Phase 2 trial called PROPEL-IPF that lists no US sites (ClinicalTrials.gov, NCT07284459). Every open study is on our IPF clinical trials page, and the admilparant drug page will be updated when results are announced.
- 1Feb 2016 Phase 2 trial, begun in January 2013, collects its last data
- 2Sep 2018 Phase 2 published: lung decline slowed, trial stopped early for gallbladder inflammation
- Jul 2020 to Aug 2022 Phase 2
- Sep 2023 to Oct 2026 ALOFT-IPF
- 3Jan 2022 BMS paper: admilparant spares the bile pumps
- 4Feb 2025 Phase 2 results published
- 5May 2026 Amendment adds liver injury as a potential risk
- 6Dec 2026 Long-term extension estimated to start
- Jan 2022 to Jul 2024 Fipaxalparant Phase 2
- 7Oct 2024 Amgen stops fipaxalparant after it misses its goals
- 8Oct 2025 FDA approves nerandomilast (Jascayd)
- 9Apr 2027 FDA decision on inhaled treprostinil for IPF, expected late April
Dates from ClinicalTrials.gov records NCT01766817, NCT04308681, NCT06003426, NCT06025578, NCT07441408 and NCT05032066, Palmer et al. (CHEST, 2018), Gill et al. (Toxicology and Applied Pharmacology, 2022), Corte et al. (AJRCCM, 2025), BioPharma Dive (amendment submitted in May 2026, day not public) and the FDA calendar. End dates for ALOFT-IPF and ALOFT-PPF are the registry's estimates.
One email when Idiopathic Pulmonary Fibrosis trials change or an FDA decision lands. No newsletter, no spam.
Admilparant Questions People Are Asking
Is admilparant safe for the liver?
It is not known yet. Bristol Myers Squibb built admilparant by reworking its earlier drug BMS-986020, which caused liver and gallbladder damage, and BMS scientists reported in 2022 that admilparant barely blocks the bile acid pumps behind that damage. Its Phase 2 trial showed no excess of serious liver or gallbladder events. In 2026 the company added liver injury as an important potential risk to the plan for its Phase 3 extension study after a limited number of liver events and 1 death, with the treatment group still blinded. The Phase 3 results should show whether liver test rises are more common on admilparant than on placebo.
When will admilparant Phase 3 results be released?
A BMS spokesperson told Fierce Biotech on October 1, 2026 that topline results for ALOFT-IPF are expected by the end of 2026 and results for ALOFT-PPF early in 2027. ClinicalTrials.gov estimated that ALOFT-IPF would finish collecting its main data on October 6, 2026, in a record last updated in March 2026, and lists an estimated December 27, 2027 completion for ALOFT-PPF in a record last updated in April 2026.
Did someone die in the admilparant trial?
Yes. The protocol amendment reported by BioPharma Dive describes 1 death from multi-organ failure involving liver injury in the ALOFT program. The person had underlying lung disease and other complications, and because the trial is still blinded, it is not known whether they were taking admilparant or placebo.
How does admilparant work?
Admilparant blocks LPA1, a receptor for lysophosphatidic acid, a fat-based signaling molecule that drives the scarring process in fibrotic lung disease. Blocking it aims to slow the scarring that steadily reduces lung capacity in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis. It is a pill taken twice a day.
What dose of admilparant is being tested?
ALOFT-IPF tests 60 mg and 120 mg twice a day against placebo for at least 52 weeks. The Phase 2 trial tested 30 mg and 60 mg twice a day for 26 weeks, and in IPF the 30 mg dose did no better than placebo.
Can I still join an admilparant trial?
Not as a new participant right now. Both Phase 3 trials, ALOFT-IPF and ALOFT-PPF, are listed as active but not recruiting. The long-term extension, estimated to start on December 16, 2026, is only for people who complete one of those trials, and it excludes anyone whose study drug was stopped permanently because of a side effect.
What happened to BMS-986020?
BMS-986020 was Bristol Myers Squibb's first LPA1 drug for IPF. Its Phase 2 trial, published in CHEST in 2018, showed slower lung function decline at 600 mg twice daily, but the drug raised liver enzymes and the trial was stopped early after 3 drug-related cases of gallbladder inflammation. BMS scientists later traced the damage to the drug blocking bile acid pumps in liver cells.
Is admilparant FDA approved?
No. Admilparant is investigational and available only inside clinical trials. The FDA-approved IPF drugs are pirfenidone, nintedanib and nerandomilast (Jascayd).
In 2022, the answer to BMS-986020 was a table of bile pump numbers in a toxicology journal. The answer to 2026 will be a different table, the rate of 3-fold liver enzyme rises on admilparant against placebo, broken out by dose, printed beside the lung function results that 1,255 people in ALOFT-IPF spent a year or more making possible. If both columns come back clean, people with IPF would have a new kind of pill to add to the ones they already take.