Certepetide
A nine-amino-acid ring injected alongside chemotherapy to open a transport route into solid tumours
Certepetide is a small cyclic peptide that does nothing to cancer cells itself. Its job is to make a tumour take up the drugs given with it. Nine amino acids, closed into a ring by a single sulfur bridge, carry two instructions in one sequence: the first sticks the peptide to integrins on the blood vessels that feed a tumour, and an enzyme cut then uncovers a second instruction that binds neuropilin-1 and switches on a transport pathway which carries fluid, and whatever is dissolved in it, out of the vessel and through tumour tissue. Because the effect works on the tumour rather than on the drug, nothing has to be chemically attached to the peptide: the chemotherapy is simply given at the same time. Laboratories have known the molecule since 2009 as iRGD, and most published work on it uses that name. Under the clinical codes CEND-1 and LSTA1, and now the approved name certepetide, it has been through a 31-patient trial with gemcitabine and nab-paclitaxel in metastatic pancreatic cancer, a randomised phase 2 trial in the same disease, a placebo-controlled trial in bile-duct cancer and a trial in glioblastoma. It is approved nowhere, and the randomised results that would settle whether the idea works in people have not been published.
Used in human trials: 3.2 mg/kg, On days 1, 8 and 15 of each 28-day cycle, Intravenous, with gemcitabine and nab-paclitaxel (Study: ASCEND randomised phase 2, pancreatic cancer) 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?
The problem certepetide was built for is mechanical rather than biological. A drug that kills pancreatic cancer cells in a dish may do very little in a patient, because a pancreatic tumour is mostly dense fibrous tissue with few, badly built vessels, and the drug never reaches most of the cells. Raising the dose raises the damage to bone marrow and nerves long before it raises the amount inside the tumour. One response to that is to attach drugs to something that homes to tumours. Certepetide came out of a different response: find a peptide that makes the tumour's own vessels leak, on purpose and only there, and then give ordinary drugs beside it.
The peptide was found by a group at the Sanford Burnham Prebys institute in La Jolla and described in 2009 under the name iRGD. Its sequence folds two signals into nine residues. The RGD motif in the middle is the classic integrin-binding sequence, which docks the peptide on the alphaV integrins that tumour vessel lining carries in quantity and healthy adult vessels largely do not. Docking is not the point of it. Once bound, the peptide is cut by an enzyme at the tumour surface, and the cut exposes a buried motif ending in arginine, the pattern that fits the neuropilin-1 receptor. Neuropilin-1 is the switch for a bulk transport route through and between cells, and once it is engaged the vessel wall and the tissue behind it become briefly permeable. In the first paper the authors showed that compounds coupled to the peptide spread through the body of a mouse tumour while the same compounds coupled to a conventional RGD peptide stopped at the vessel wall.
The finding that made a drug of it came a year later. Injecting the peptide on its own, with nothing attached, raised the uptake of whatever drug was given with it: a small molecule (doxorubicin), two nanoparticle drugs (nab-paclitaxel and liposomal doxorubicin) and an antibody (trastuzumab) all worked better in mice without being chemically changed. That is unusual and commercially awkward in equal measure, because it means the peptide cannot be sold as part of a drug; it has to be added to someone else's. It also means the peptide can in principle be dropped into an existing regimen without reformulating anything, which is exactly how every human trial has used it.
Three other effects have been reported in animals, and the developer describes all of them as part of the mechanism. The peptide slows the spread of tumours in mice, an effect that depends on the neuropilin-binding half of the sequence rather than the integrin-binding half, and that shows up in the laboratory as tumour cells retracting their processes and crawling away from the peptide. It changes the mix of immune cells inside a tumour. And the transport it opens runs both ways: injecting it into mice with small liver tumours pushed tumour markers out into the blood, enough to make a borderline blood test positive, which is a diagnostic idea rather than a treatment. How much any of this contributes in a person is unknown.
In people the peptide has been given to a few hundred patients, always with chemotherapy. The first-in-human trial, at three Australian hospitals between 2018 and 2019, escalated single doses from 0.2 to 3.2 mg/kg during a one-week run-in and then gave the peptide with gemcitabine and nab-paclitaxel to 31 patients with metastatic pancreatic cancer. Nothing in the escalation limited the dose. Seventeen of 29 evaluable patients had their tumours shrink, one of them completely, and median survival was 13.2 months. A single-arm trial cannot show that any of this came from the peptide, and the authors said so: they called the activity encouraging and asked for randomised trials.
Those trials have been run and their results are, at the time of writing, not in the literature. ASCEND, run by the Australasian Gastro-Intestinal Trials Group, randomised patients with untreated metastatic pancreatic cancer two to one between 3.2 mg/kg of the peptide and placebo on top of the same chemotherapy, in two cohorts that differed only in whether a second dose followed four hours later; its protocol paper sets progression-free survival as the primary endpoint and a sample size of 155. BOLSTER tested the same amount against placebo in 66 patients with bile-duct and gallbladder cancer in the United States, with adverse events as its primary endpoint; its results are posted on the trial registry and show the usual burden of advanced cancer in both arms, with serious adverse events and deaths in similar proportions on peptide and on placebo. A phase 2a trial in newly diagnosed glioblastoma is running in Estonia and Latvia with overall survival as its endpoint, and a licensee has run two trials in China. The developer, Lisata Therapeutics, has described preliminary signals from ASCEND in its own filings, including four complete responses against none on placebo in the first cohort; that is the company's account of unpublished data, not a peer-reviewed result.
What a careful reader should take from this is that the idea is well evidenced in mice, that the peptide appears to add little toxicity of its own to a harsh chemotherapy backbone, and that the question of whether patients live longer is still open. The company's most recent quarterly filing says it has deferred the manufacturing work needed for a phase 3 trial in pancreatic cancer to conserve cash, and two registered trials were withdrawn before enrolling anyone. No regulator has approved the peptide for anything, and the designations it holds in the United States and Europe are development incentives rather than evidence that it works.
Mechanism of Action
The peptide is a switch, not a poison. Its sequence binds one receptor to get to the tumour, is then cut to reveal a second binding site, and the second receptor opens a bulk transport route that carries co-injected drugs out of the vessel and through the tissue. Two further effects, on metastasis and on the immune cells inside a tumour, have been shown in animals.
Binds alphaV integrins on tumour vessels
The RGD motif docks the peptide on the integrins that new tumour vessel lining carries in quantity and that quiet adult vessels largely do not, which is what makes the rest of the sequence act where a tumour is (PMID 19962669).
Is cut, uncovering a neuropilin-1 binding motif
Enzymes at the tumour surface cut the bound peptide, and the cut exposes a buried motif ending in arginine. The truncated peptide loses its grip on the integrin and binds neuropilin-1 instead (PMIDs 19962669, 23151901).
Opens a transport route through vessel and tissue
Engaging neuropilin-1 turns on a bulk transport pathway that briefly makes the tumour vessel wall and the tissue behind it permeable, so drugs injected at the same time reach cells they would otherwise never meet. One dose keeps a mouse tumour penetrable for at least 24 hours (PMIDs 20378772, 36982773).
Needs no chemistry with the drug it helps
The effect is on the tumour, so a small molecule, a nanoparticle drug and an antibody were all carried in better simply by being injected alongside the peptide. This is why it is added to existing regimens rather than formulated into them (PMID 20378772).
Repels tumour cells and slows spread in mice
The neuropilin-binding half of the sequence, not the integrin-binding half, stops tumour cells migrating, makes them retract their processes and reduces spontaneous metastasis in mice (PMID 25392370).
Runs in both directions
The route it opens also lets tumour contents into the blood: one injection raised blood tumour markers in mice with small liver or prostate tumours, an effect blunted by blocking neuropilin-1 (PMID 38889481).
Published Research
The studies below were read from their PubMed abstracts on November 4, 2026: the five human reports (one completed trial, two pharmacokinetic analyses and two protocols for trials whose results are not yet published), the two mouse papers that established what the peptide does, and five further animal and cell studies. Most of the published literature on this molecule is about nanoparticles, antibodies and cells with the peptide chemically attached to them. Those are different products under our rule that a card follows the molecule tested, and they are listed under References; the cards here are studies that gave the peptide itself, whether alone or beside another drug. Two cards are for papers whose titles name neither the peptide nor any of its names, and each carries a relevance-sweep record quoting the words in its abstract that do.
First-in-human phase 1 with gemcitabine and nab-paclitaxel
Thirty-one adults with untreated metastatic pancreatic ductal adenocarcinoma at three Australian hospitals were given the peptide as an intravenous bolus, first alone during a seven-day run-in at doses rising from 0.2 to 3.2 mg/kg, then on days 1, 8 and 15 of 28-day cycles with gemcitabine 1,000 mg/m2 and nab-paclitaxel 125 mg/m2 until the disease progressed. No dose limited the escalation. The commonest severe events were the ones the chemotherapy pair is known for: low neutrophils in 55% of patients, anaemia in 26%, low white cells in 16% and pulmonary embolism in 13%. Serious events occurred in 71%, mostly from the cancer itself, and ten patients died during the study, nine from progressive disease and one from a stroke. Of 29 patients assessed for response, 17 (59%) had tumour shrinkage, including one complete response, and median overall survival was 13.2 months (95% CI 9.7 to 22.5) after a median 26 months of follow-up. The authors concluded that randomised trials were warranted. The trial was funded by the developer.
Pharmacokinetics in four animal species and in patients
Infused intravenously, the peptide left the blood quickly: a half-life of roughly 25 minutes in mice and about 2 hours in patients with metastatic pancreatic cancer. A tritium-labelled version given to mice bearing mammary tumours appeared in the tumour and in several healthy tissues within minutes, but had cleared from most healthy tissue by three hours while a substantial amount stayed in the tumour. In mice with liver cancer, the tumour stayed penetrable to injected contrast agents and dyes for at least 24 hours after one dose. The authors read this as a short blood exposure buying a much longer window for the drugs given with it.
Population pharmacokinetics in patients
Concentration measurements from patients with metastatic pancreatic cancer receiving the peptide with nab-paclitaxel and gemcitabine fitted a two-compartment model with linear elimination. Body weight affected the volumes of distribution and kidney function affected clearance: as creatinine clearance fell, clearance of the peptide fell and exposure rose, and the authors flagged both a body weight of 100 kg and a creatinine clearance of 50 or 150 mL/min as potentially meaningful for exposure. The analysis exists to inform dose choice in later trials; it reports no clinical outcome.
ASCEND: protocol for the randomised phase 2 trial in pancreatic cancer
The design paper for the trial that is meant to answer the efficacy question. Patients with untreated advanced pancreatic ductal adenocarcinoma are randomised 2:1 to gemcitabine 1,000 mg/m2 and nab-paclitaxel 125 mg/m2 with either 3.2 mg/kg of the peptide or placebo on days 1, 8 and 15 of each 28-day cycle until progression; an amendment added a second cohort in which a second dose follows four hours after chemotherapy. The planned sample size is 155, powered to detect a rise in six-month progression-free survival from 16% to 63%, with response rate, safety, overall survival, patient-reported outcomes and tissue biomarkers as further endpoints. The paper also reports the figure that justified the trial: in the phase 1b setting, 3.2 mg/kg with the same chemotherapy gave a 92% disease control rate at 16 weeks. No results are in it.
Protocol for the glioblastoma phase 2a trial
An exploratory, double-blind, placebo-controlled trial in newly diagnosed glioblastoma, sponsored by Tartu University Hospital, funded by the developer and running at hospitals in Estonia and Latvia. After surgery and radiotherapy with concurrent temozolomide, 30 subjects are randomised 2:1 to intravenous peptide or placebo alongside six cycles of adjuvant temozolomide, with overall survival as the primary endpoint. The first subject was enrolled in January 2024 and recruitment was still open when the protocol was published. This is the peptide's first test inside the skull; no results are reported.
Discovery: a peptide that carries cargo through tumour tissue
The paper that described the molecule, under the name iRGD. Compounds coupled to it and injected into the veins of tumour-bearing mice bound the tumour vessels and then spread out into the tissue beyond them, while the same compounds on a conventional RGD peptide stayed at the vessel wall. The authors worked out the three steps: the RGD motif binds alphaV integrins on tumour endothelium, an enzyme cut then exposes a motif that binds neuropilin-1, and that binding drives penetration into tissue and into cells. Coupling improved both a tumour imaging agent and an anticancer drug.
The co-administration result: nothing needs to be attached
In mouse tumour models the peptide raised the permeability of vessels and tissue in a way that was specific to tumours and depended on neuropilin-1, and drugs given at the same time crossed into the tumour tissue without being chemically joined to the peptide. Injecting it improved the therapeutic index of four very different agents: doxorubicin, nab-paclitaxel, liposomal doxorubicin and the antibody trastuzumab. This is the result the whole clinical programme rests on, and it is the reason the peptide is given as a separate injection beside standard chemotherapy rather than built into a drug.
Metastasis slowed in mice, through the neuropilin half of the sequence
The peptide strongly reduced spontaneous metastasis in mice. The effect came from the neuropilin-binding motif and not from the integrin-binding RGD motif, which separates it from the drug-delivery function the RGD part begins. In culture the peptide stopped tumour cells migrating and actively repelled them: cells pulled in their processes and partly detached, most clearly when they had been grown on fibronectin. The authors suggested this would be an additional benefit when the peptide is used for delivery.
Co-administered with an antibacterial peptide in colon cancer models
A peptide derived from a Helicobacter pylori ribosomal protein was tested on colon cancer cell lines and in mouse isografts, alone and with this peptide and with fluorouracil. Giving the two peptides together increased cell death over either alone, and adding fluorouracil raised p53 with the expected shifts in the genes it controls. The combination of the two peptides significantly reduced tumour size and weight, and adding fluorouracil increased dead tissue and reduced fibrous tissue inside the tumours. The cargo here is another experimental peptide rather than a registered drug, so the result is about the delivery principle, not about a treatment.
Co-administration against conjugation in a brain tumour model
Doxorubicin carried on a dendrimer polymer was tested in rat glioma cells and in mice, either with the peptide chemically attached to the carrier or with the peptide simply injected alongside it. Both penetrated tumour spheroids further than a conventional RGD peptide did (150 and 144 micrometres against 115), and co-administration did at least as well as conjugation throughout: median survival was 61 days when the peptide was co-administered, 57.5 days when it was conjugated and 43.5 days with the conventional RGD conjugate. The carrier is a different product, but the co-administration arm tested this peptide as it is used clinically.
The same transport running the other way, out of the tumour
Injected into the veins of mice with liver cancer, the peptide quickly and substantially raised blood levels of alpha-fetoprotein, a tumour marker, while doing nothing of the kind in mice with chronic liver injury and no tumour. The effect was largest in animals with small tumours and normal baseline marker levels, was blunted by an antibody against neuropilin-1, and tracked the concentration difference between tumour and blood. The same thing happened with a second liver marker and with prostate-specific antigen in mice with prostate cancer. The authors propose this as a way to make blood tests detect early tumours, which is a diagnostic use of the peptide rather than a treatment.
Used as a neuropilin-1 activator outside cancer
A study of steroid-induced bone death in the hip, in human and rat samples and in cultured cells, identified neuropilin-1 as a control point in how T cells release interferon gamma and how bone marrow stromal cells then build bone. The peptide was used as the pharmacological way to switch neuropilin-1 on, and doing so changed interferon gamma release and the signalling downstream of it. The finding is about the receptor rather than about the drug, but it is a reminder that the receptor this peptide engages is not confined to tumours.
Dosing Data
Every amount below was given inside a clinical trial, by injection into a vein, to patients with advanced cancer who were also receiving chemotherapy. There is no approved product and no label, so there is no recommended dose. The amount settled on early and did not move: 3.2 mg/kg was the top of the phase 1 escalation and the dose used in every phase 2 trial since, given on each day chemotherapy is given. The registry record of the bile-duct cancer trial describes it as a slow push over about a minute; one cohort of the ASCEND trial added a second identical dose four hours after chemotherapy, to test whether a longer open window helps. Because the peptide is cleared partly by the kidneys and exposure rises when kidney function falls, trial protocols required adequate renal function.
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 Certepetide 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: intravenous, intravenous bolus). 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 Certepetide, 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 Certepetide stays intact once mixed.
How it is taken
As it was given in human studies: Intravenous, with gemcitabine and nab-paclitaxel (On days 1, 8 and 15 of each 28-day cycle; Study: ASCEND randomised phase 2, pancreatic cancer); Intravenous (A second dose four hours after chemotherapy, on the same days; Study: ASCEND second cohort, a repeat dose); Intravenous bolus (A single bolus in a seven-day run-in, then weekly for three weeks of four; Study: phase 1 dose escalation, peptide alone then with chemotherapy).
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 About 2 hours in patients; about 25 minutes in mice. After about five half-lives almost none is left.
How long the doses were given: Study: ASCEND randomised phase 2, pancreatic cancer: Until the disease progressed; Study: ASCEND second cohort, a repeat dose: Until the disease progressed; Study: phase 1 dose escalation, peptide alone then with chemotherapy: One escalation cycle, then expansion.
When effects appear: unknown; no source on this page gives a time to effect for Certepetide. Results reported in the studies are under Published Research.
Source: half-life: PMID 36982773; 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 dose-limiting toxicity at any dose up to 3.2 mg/kg in the phase 1 trial, and adverse events generally consistent with what gemcitabine and nab-paclitaxel cause on their own (PMID 35803294); Severe low neutrophil counts in 55% of the 31 phase 1 patients, anaemia in 26%, low white cells in 16% and pulmonary embolism in 13%: the recognised toxicity of that chemotherapy pair (PMID 35803294); Serious adverse events in 71% of phase 1 patients, mostly attributed to the cancer progressing; ten deaths during the study, nine from progressive disease and one from a stroke (PMID 35803294); In the placebo-controlled bile-duct cancer trial, serious adverse events in 10 of 23 patients on the peptide against 12 of 21 on placebo in the untreated group, and 3 of 11 against 4 of 11 in the second-line group; deaths were 12 against 10 and 4 against 2 (ClinicalTrials.gov NCT05712356, posted results); Exposure rises as kidney function falls, which is a reason for the renal-function entry criteria in the trials rather than a reported harm (PMID 39789733); The developer states that pooled ASCEND data showed no increase in adverse events beyond standard of care; that is the company's account of data it has not published (Lisata Therapeutics, 2025). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Certepetide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Every person who has received this peptide was having chemotherapy at the same time, and most had advanced pancreatic or bile-duct cancer, so almost nothing below can be pinned on the peptide alone”).
Interactions
- gemcitabine and nab-paclitaxel: co-administration is the point of the drug, not a hazard to avoid: in 31 patients the peptide was given on each chemotherapy day with no dose-limiting toxicity and a side-effect pattern the authors judged consistent with the chemotherapy pair alone
- impaired kidney function (not a drug interaction, recorded here because it changes exposure): clearance falls and exposure rises as creatinine clearance falls, which is why trials required adequate renal function; body weight affects the volumes of distribution
Every peptide's record, with its source: the interaction matrix.
Source: human study, PMID 35803294; human study, PMID 39789733.
Checking what you bought
Unknown: no published independent test of Certepetide 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 Certepetide's expected mass, 948.0 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
Every person who has received this peptide was having chemotherapy at the same time, and most had advanced pancreatic or bile-duct cancer, so almost nothing below can be pinned on the peptide alone. What the trials can say is whether adding it made things worse.
Contraindications & Cautions
There is no label, so there are no official contraindications. These follow from how the trials were run and what the peptide does.
Legal Status
Certepetide is an investigational drug. It is approved nowhere, and the designations it holds are incentives for developing a drug for a rare or serious disease, not findings that it works.
Frequently Asked Questions
?What is certepetide?
A nine-amino-acid cyclic peptide, known in the laboratory literature as iRGD and in trials as CEND-1 or LSTA1. It is given into a vein alongside chemotherapy, and its purpose is to make the tumour take up the chemotherapy rather than to attack the tumour itself.
?How can a drug work by doing nothing to the cancer?
It works on the tumour's plumbing. The peptide binds integrins on tumour blood vessels, is cut there, and the cut piece binds neuropilin-1, which switches on a transport route that briefly makes the vessel wall and the surrounding tissue permeable. Anything in the bloodstream at that moment, including a chemotherapy drug given at the same time, gets carried in with it.
?Does it have to be attached to the drug?
No, and that is the central finding. In mice, injecting the peptide on its own improved the effect of doxorubicin, nab-paclitaxel, liposomal doxorubicin and trastuzumab without any chemical link between them. Every human trial has given it as a separate injection beside standard chemotherapy.
?Did it help patients live longer?
Not demonstrated. The single-arm phase 1 trial in metastatic pancreatic cancer reported tumour shrinkage in 59% of assessable patients and median survival of 13.2 months, which its authors called encouraging, but a trial without a control group cannot say what the peptide added. The randomised trials that could answer the question have been run, and the developer has described encouraging preliminary signals in its own filings; no randomised result has been published.
?Is it the same as the iRGD nanoparticles in the research literature?
The peptide is the same molecule, but those are different products. Most papers that mention iRGD describe it chemically attached to a nanoparticle, a liposome, an antibody or a cell surface. Findings about those belong to the thing that was built, and this page lists them under References rather than as studies of this drug.
?Why is the dose in milligrams per kilogram?
Because it was developed as a hospital infusion for adults with cancer, where dosing by body weight is normal, and because body weight turned out to affect how the peptide distributes. The population pharmacokinetic analysis found weight affecting the volumes of distribution and kidney function affecting clearance.
?Can anyone buy it?
No. It exists only as a trial product, made up by hospital pharmacies and given with chemotherapy that requires a cancer centre. Grey Peptides sells nothing and links to no vendor; a product sold under this name outside a trial would not be the trial drug.
References
- [clinical-trial] Dean A, et al. "Dual αV-integrin and neuropilin-1 targeting peptide CEND-1 plus nab-paclitaxel and gemcitabine for the treatment of metastatic pancreatic ductal adenocarcinoma: a first-in-human, open-label, multicentre, phase 1 study." Lancet Gastroenterol Hepatol, 2022;7(10):943-951. PMID: 35803294.
- [pubmed] Järveläinen HA, et al. "Assessment of the Pharmacokinetics, Disposition, and Duration of Action of the Tumour-Targeting Peptide CEND-1." Int J Mol Sci, 2023;24(6). PMID: 36982773.
- [clinical-trial] Winning A, et al. "Population Pharmacokinetic Modeling of Certepetide in Human Subjects With Metastatic Pancreatic Ductal Adenocarcinoma." Clin Pharmacol Drug Dev, 2025;14(3):240-251. PMID: 39789733.
- [clinical-trial] Lee J, et al. "ASCEND: a randomised, double-blinded, placebo-controlled, phase II study of gemcitabine and nab-paclitaxel with LSTA1 in untreated metastatic pancreatic adenocarcinoma. An Australasian Gastro-Intestinal Trials Group (AGITG) trial." ESMO Gastrointest Oncol, 2023;1:3-8. PMID: 41647283.
- [clinical-trial] Truusalu JP, et al. "LSTA1-GBM-2A: study protocol for an exploratory phase 2a randomised controlled trial evaluating tumour-homing peptide certepetide with temozolomide in glioblastoma multiforme." BMJ Open, 2025;15(11):e106094. PMID: 41248393.
- [pubmed] Sugahara KN, et al. "Tissue-penetrating delivery of compounds and nanoparticles into tumors." Cancer Cell, 2009;16(6):510-20. PMID: 19962669.
- [pubmed] Sugahara KN, et al. "Coadministration of a tumor-penetrating peptide enhances the efficacy of cancer drugs." Science, 2010;328(5981):1031-5. PMID: 20378772.
- [pubmed] Sugahara KN, et al. "Tumor-penetrating iRGD peptide inhibits metastasis." Mol Cancer Ther, 2015;14(1):120-8. PMID: 25392370.
- [pubmed] Yaghoubi A, et al. "Anticancer activity of Helicobacter pylori ribosomal protein (HPRP) with iRGD in treatment of colon cancer." J Cancer Res Clin Oncol, 2021;147(10):2851-2865. PMID: 34117917.
- [pubmed] Wang K, et al. "Tumor penetrability and anti-angiogenesis using iRGD-mediated delivery of doxorubicin-polymer conjugates." Biomaterials, 2014;35(30):8735-47. PMID: 25023394.
- [pubmed] Schmithals C, et al. "Tumour-specific activation of a tumour-blood transport improves the diagnostic accuracy of blood tumour markers in mice." EBioMedicine, 2024;105:105178. PMID: 38889481.
- [pubmed] Lu H, et al. "Targeting the neuropilin 1/interferon γ axis restores glucocorticoid-suppressed T cell function and rescues bone formation to prevent steroid-induced osteonecrosis." Bone Joint Res, 2026;15(7):795-810. PMID: 42413921.
- [pubmed] Qiu F, et al. "[(68)Ga]Ga-DOTA-CEND1: A Novel PET Cyclic Peptide Tracer for Noninvasive Imaging of Neuropilin-1 Expression in Pan-Tumors." Mol Pharm, 2026;23(1):361-372. PMID: 41324177.
- [pubmed] Zhu M, et al. "Combination Therapy with iRGD-antiCD3 and PD-1 Blockade Enhances Antitumor Potency of Cord Blood-Derived T Cells." Onco Targets Ther, 2021;14:835-844. PMID: 33574677.
- [pubmed] Song G, et al. "iRGD Tumor Penetrating Peptide-Modified NK Cells Exhibit Enhanced Tumor Immune Infiltration Ability and Anti-Tumor Efficacy." Protein Pept Lett, 2025;32(3):183-193. PMID: 39950266.
- [pubmed] Shao J, et al. "Combining iRGD with HuFOLactis enhances antitumor potency by facilitating immune cell infiltration and activation." Hum Vaccin Immunother, 2024;20(1):2375825. PMID: 39101772.
- [pubmed] Simón-Gracia L, et al. "iRGD peptide conjugation potentiates intraperitoneal tumor delivery of paclitaxel with polymersomes." Biomaterials, 2016;104:247-57. PMID: 27472162.
- [pubmed] Hamilton AM, et al. "Nanoparticles coated with the tumor-penetrating peptide iRGD reduce experimental breast cancer metastasis in the brain." J Mol Med (Berl), 2015;93(9):991-1001. PMID: 25869026.
- [pubmed] Alberici L, et al. "De novo design of a tumor-penetrating peptide." Cancer Res, 2013;73(2):804-12. PMID: 23151901.
- [pubmed] Liu X, et al. "Targeted drug delivery using iRGD peptide for solid cancer treatment." Mol Syst Des Eng, 2017;2(4):370-379. PMID: 30498580.
- [pubmed] Ma G, et al. "Tumor-homing peptides in precision oncology." J Control Release, 2026;399(Pt A):115360. PMID: 42749136.
- [pubmed] Di ME, et al. "Anticancer Peptides: Design Principles, Translational Bottlenecks, and Emerging Opportunities." Molecules, 2026;31(18). PMID: 42796603.
- [pubmed] Springfeld C, et al. "CEND-1: a game changer for pancreatic cancer chemotherapy?." Lancet Gastroenterol Hepatol, 2022;7(10):900-902. PMID: 35803295.
- [registry] ClinicalTrials.gov API v2, read November 4, 2026: eight records name the peptide as certepetide, CEND-1 or LSTA1. NCT03517176 (phase 1, Lisata Therapeutics, 30 enrolled, July 2018 to June 2020, completed, no results posted) is the first-in-human study. NCT05042128 (ASCEND, Australasian Gastro-Intestinal Trials Group, phase 2, 158 planned, started April 2022, status last updated October 2024, no results posted). NCT05712356 (BOLSTER, phase 2a in cholangiocarcinoma and gallbladder cancer, Lisata, 66 enrolled at 19 US sites, May 2023 to April 2026, completed WITH results posted). NCT05121038 (CENDIFOX, investigator-sponsored, phase 1b/2a with FOLFIRINOX in pancreatic, colon and appendiceal cancer). NCT05052567 (Qilu Pharmaceutical, phase 1b/2, China, 50 enrolled, completed June 2024) and NCT06261359 (Qilu, phase 2, 120 planned). Two records were withdrawn without enrolling anyone: NCT06592664 (FORTIFIDE, phase 1b/2a) and NCT06216561 (an intraperitoneal phase 1 at the University of California, San Diego). https://clinicaltrials.gov/study/NCT03517176
- [registry] ClinicalTrials.gov NCT05712356 (BOLSTER), posted results read November 4, 2026: patients were enrolled from May 2023 to February 2025 at US sites and given 3.2 mg/kg by slow intravenous push over one minute, or placebo, on each day standard treatment was given. Untreated cholangiocarcinoma: 23 on the peptide with durvalumab, cisplatin and gemcitabine against 21 on placebo; serious adverse events in 10 of 23 against 12 of 21, deaths in 12 against 10. Second-line disease with FOLFOX: 11 against 11; serious adverse events in 3 against 4, deaths in 4 against 2. https://clinicaltrials.gov/study/NCT05712356
- [other] FDA Global Substance Registration System, substance Certepetide, UNII 7PF4546T2P: a complete nine-residue peptide, sequence CRGDKGPDC, with one disulfide bridge from residue 1 to residue 9 (read November 4, 2026). https://gsrs.ncats.nih.gov/
- [other] ChEMBL molecule CHEMBL5315026 (CERTEPETIDE): molecule type protein, highest clinical phase 2, USAN stem -tide assigned in 2023, synonyms CEND-1, LSTA1 and LSTA-1 (read November 4, 2026). https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL5315026/
- [other] openFDA, read November 4, 2026: the Drugs@FDA and drug label endpoints return no record for certepetide, LSTA1 or CEND-1, so the peptide has no US approval and no US label.
- [other] Lisata Therapeutics, Inc., quarterly report on Form 10-Q for the quarter ended June 30, 2026 (filed with the US Securities and Exchange Commission, read November 4, 2026): the company states that certepetide is or has been the subject of several phase 2 studies in metastatic pancreatic cancer, cholangiocarcinoma, appendiceal cancer, colon cancer and glioblastoma, and that it has delayed readiness work, including chemistry, manufacturing and controls, for a planned phase 3 study in metastatic pancreatic cancer in order to conserve capital. https://www.sec.gov/Archives/edgar/data/0000320017/000032001726000038/lsta-20260630.htm
- [other] Lisata Therapeutics, Inc., quarterly results release for the first quarter of 2025 (exhibit 99.1 to its SEC filing, read November 4, 2026), the company's own account of its programme: ASCEND cohort A gave 95 patients a single 3.2 mg/kg dose and cohort B gave 63 patients two 3.2 mg/kg doses four hours apart; preliminary cohort A data presented in January 2025 showed a positive trend in overall survival and four complete responses against none on placebo. The release lists US fast track designation in pancreatic cancer, US orphan drug designation in pancreatic cancer, glioma, osteosarcoma and cholangiocarcinoma, EU orphan designation in pancreatic cancer and US rare paediatric disease designation in osteosarcoma. None of these figures has been published in a peer-reviewed report. https://www.sec.gov/Archives/edgar/data/0000320017/000032001725000028/ex991earningsrelease1q25fi.htm
Sources & Citations
Every study on this page was read from its PubMed record on November 4, 2026. The sequence and disulfide come from the FDA Global Substance Registration System, the development phase from ChEMBL, the trial records and the bile-duct trial's posted results from ClinicalTrials.gov, and the absence of a US approval from openFDA, all read the same day. Where a figure has only the developer's word behind it, the page says so and names the company and the filing. Grey Peptides sells nothing and links to no vendor.
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