Satoreotide Tetraxetan
A receptor-blocking peptide that carries radiation to neuroendocrine tumours
Satoreotide tetraxetan is JR11, a synthetic peptide that sits on somatostatin receptor 2 without switching it on, with a DOTA cage that holds a radioactive metal. Most radioligand therapy for neuroendocrine tumours uses agonists such as dotatate, which the cell pulls inside; this antagonist stays on the surface but finds more receptors. With lutetium-177 it has been tested in about a hundred patients across small trials, with promising tumour control and more blood-count side effects than standard treatment. It is an investigational hospital radiopharmaceutical.
Used in human trials: 4.5 GBq with 300 µg peptide, Per cycle, Intravenous (Lutetium-177 satoreotide tetraxetan, phase 1/2 part A) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
Many neuroendocrine tumours carry large numbers of somatostatin receptor 2 on their surface. Since the 2000s the standard way to treat them with radiation from inside has been to attach lutetium-177 to an agonist peptide, octreotate or octreotide, which the cell takes in once it binds. Antagonists bind without triggering uptake, and the idea behind them is that they may still deliver more radiation because they recognise more receptor sites. JR11 is the antagonist that was taken into clinical development, and satoreotide tetraxetan is JR11 with a DOTA chelator, also called DOTA-JR11 or OPS201. Its imaging partner, satoreotide trizoxetan, uses the same peptide with a NODAGA chelator.
Laboratory work supports the idea. In cells carrying the human receptor, the lutetium-labelled antagonist recognised about four times as many binding sites as lutetium dotatate, bound faster and let go more slowly, and stayed mostly on the surface. In mice it gave a higher tumour dose, caused more DNA damage in tumour cells and delayed tumour growth longer than the agonist. Raising the amount of unlabelled peptide in the injection lowered doses to the liver and marrow without saturating the tumour, which agonists do.
In people, a 2014 pilot in four patients found tumour doses 1.7 to 10.6 times higher than with lutetium dotatate in the same patients. A phase 1 trial in 20 heavily treated patients gave up to 7.4 GBq per cycle: 45% responded and median progression-free survival was 21 months, but four of seven patients had grade 4 blood-count toxicity after the second cycle, and the protocol was changed to cap the bone-marrow dose at 1 Gy. Ipsen's phase 1/2 study in 40 patients then used dosimetry to keep kidney and marrow doses under set limits; disease control was 94.7% and the response rate 21.1%, 42.5% had grade 3 or worse treatment-related side effects, mostly low blood counts, and two developed myeloid neoplasms judged treatment related.
Smaller academic studies have since used it after standard treatment fails. Patients with meningioma or paraganglioma, and neuroendocrine tumour patients who progressed early after lutetium-177 DOTATOC, received the antagonist after the agonist; tumour doses per cycle were 1.3 to about 2 times higher, and progression-free survival was longer than before, in groups of 6 to 15 people. These are retrospective or uncontrolled comparisons, and a 2026 critical review of antagonist radioligands points out that no prospective trial has yet shown a survival benefit and that blood toxicity is higher than with agonists.
The same molecule labelled with gallium-68 has been tested for PET. It showed fewer normal-organ signals and more liver metastases than gallium-68 dotatate, but fewer bone lesions, and it missed more of the small tumours that cause tumour-induced osteomalacia. Satoreotide tetraxetan is prepared in hospital radiopharmacies for trials. It has no FDA or EMA approval, and it is not something anyone can buy or use outside a nuclear-medicine department.
Mechanism of Action
The peptide does not treat the tumour by itself. It is a carrier: it finds somatostatin receptor 2 on tumour cells and holds the radioactive metal there.
Receptor antagonism
Binds somatostatin receptor 2 without activating it; in cells it saw four times as many binding sites as lutetium dotatate (2021 study).
Surface retention
Most of it stays on the cell surface instead of being taken in, and it dissociates slowly, so tumour residence is long (2021 and 2017 studies).
Lutetium-177 radiation
Beta particles from lutetium-177 damage tumour DNA; tumours received a median 5.0 Gy per GBq in patients (2024 study).
Bone marrow exposure
Marrow dose per GBq is higher than with agonists, which is why trials cap it and why low blood counts are the main side effect (2019 and 2023 studies).
Published Research
These studies were read from their PubMed abstracts on October 29, 2026: twelve in patients, six in animals or cells and two reviews. Gallium-68 and actinium-225 forms of DOTA-JR11 are the same molecule with a different metal and are carded here. Four patient studies and one mouse study are titled only for 'somatostatin receptor antagonists' and are carded because their abstracts name DOTA-JR11 as the drug given.
Phase 1/2: 40 patients with progressive NETs
Fifteen patients had three fixed cycles of 4.5 GBq with 300 µg peptide; 25 more had one to five cycles at 4.5 or 6.0 GBq within dose caps of 23 Gy to the kidneys and 1.5 Gy to marrow. Disease control was 94.7% and the response rate 21.1%. Grade 3 or worse treatment-related events, mainly low lymphocytes, platelets and neutrophils, hit 42.5%; no severe kidney toxicity; two treatment-related myeloid neoplasms.
Dosimetry from the phase 1/2 study
Uptake peaked by the first scan at 4 hours and then fell exponentially. The kidneys cleared 57-66% of the activity within 48 hours. Median terminal blood half-life was 127 hours. Per GBq, tumours received 5.0 Gy, kidneys 0.9, spleen 0.8, liver 0.2 and marrow 0.1 Gy; after three cycles marrow had 1.1 Gy and kidneys 10.8 Gy.
Phase 1 in 20 patients
Twenty patients with advanced NETs had a dosimetry scan, then the safe activity in two cycles three months apart, up to 7.4 GBq each. After cycle 2, four of seven had grade 4 blood toxicity, so the study paused and capped marrow dose at 1 Gy and halved cycle 2. Best response was 45% (one complete, eight partial); median progression-free survival was 21.0 months.
First treatment pilot: antagonist vs dotatate
Four patients received about 1 GBq of each drug for dosimetry. The antagonist gave 1.7 to 10.6 times the tumour dose of lutetium dotatate, with better tumour-to-kidney and tumour-to-marrow ratios. All four were then treated with it: two partial remissions, one stable and one mixed response, with minor reversible side effects.
PROMENADE: refractory meningioma
Six patients had one cycle of lutetium-177 DOTATOC (about 7 GBq), then two or three cycles of the antagonist at 2 GBq per m2 (3.3-4.9 GBq). Median meningioma dose per cycle was 11.5 Gy against 3.4 Gy, with higher marrow and kidney doses but better ratios. Three had reversible grade 3 low blood counts; disease control at 12 months was 83%.
Rechallenge after early progression on DOTATOC
Fifteen NET patients who progressed within 12 months of standard DOTATOC therapy got one or two DOTATOC cycles plus one or two antagonist cycles (2.8-4.8 GBq). Median progression-free survival was 14 months against 11 after the earlier treatment (hazard ratio about 0.34). Tumour dose per cycle was 18.5 Gy against 12.9 Gy; no grade 4 events.
Metastatic pheochromocytoma and paraganglioma
Six patients in a retrospective pilot had DOTATOC first and then the antagonist at 2 GBq per m2. Median tumour dose per cycle was 1.3 times higher with the antagonist. Progression-free survival after it was 12.5 months, against 3.5 months before entry. The worst side effect was grade 3 lymphopenia in one patient.
Gallium-68 PET predicts lutetium-177 dose
In 20 patients, 95 lesions were compared on gallium-68 DOTA-JR11 PET and lutetium-177 SPECT. Uptake measures correlated only modestly (r 0.3-0.7), but even lesions with low PET uptake took up much more of the lutetium form. The authors concluded low PET uptake should not exclude treatment.
Gallium-68 DOTA-JR11: biodistribution and dose
Twenty patients were scanned an hour after about 169 MBq. Unlike agonists, there was little uptake in the pituitary, spleen, adrenals and normal liver. Tumour uptake plateaued by 20-30 minutes. The effective dose was 0.022 mSv per MBq, with the bladder wall and kidneys most exposed.
Gallium-68 DOTA-JR11 vs DOTATATE PET
In 31 patients scanned on consecutive days, the antagonist found more liver lesions (552 vs 365) with better contrast but fewer bone lesions (158 vs 388). Normal-organ uptake was lower. The authors noted the gallium-labelled form binds the receptor less tightly than the lutetium form.
Gallium-68 DOTA-JR11 PET in meningioma
Of 36 patients with suspected meningioma, 32 were confirmed. PET found 31 meningiomas, uptake was much higher than in other tumours, and it showed bone involvement in all 14 proven cases against 11 on MRI. Overall accuracy did not differ significantly from contrast MRI.
Tumour-induced osteomalacia: DOTATATE did better
Nineteen patients with this rare tumour-driven bone disease had both scans. Gallium-68 DOTATATE found the culprit tumour in 18 and DOTA-JR11 in 11 (94.7% vs 57.9%), though the antagonist helped pick the right lesion when DOTATATE showed several.
Mice: higher tumour dose than dotatate
Lutetium-177 OPS201 stayed in tumours 15.6 hours against 6.4 for lutetium dotatate, giving 2.5 times the tumour dose. Increasing the peptide from 10 to 2,000 pmol did not saturate tumours, and going to 200 pmol cut the effective dose about fivefold. Lysine or gelatine infusions lowered kidney dose by 25-45%.
Repeated cycles in mice vs dotatate
The antagonist saw twice as many receptor sites as lutetium dotatate in vitro. Given weekly for four weeks at 15 MBq, it delayed tumour growth to the endpoint size to a median 68 days, against 43 and 48 days for dotatate at 15 and 30 MBq, with mild effects on weight, blood and kidneys.
Agonist vs antagonist therapy in mice
Cells took up five times more of the antagonist, 88% of it on the membrane, and showed twice as many DNA breaks. In tumour-bearing mice, median survival was 71 days with the antagonist, 61 with lutetium octreotate and 43.5 untreated.
Two treatment cycles in a pancreatic NET model
Mice with tumours carrying the human receptor received two injections three weeks apart. The antagonist shrank tumours and extended median survival to 207 days against 126 for lutetium DOTATOC, with four times the tumour uptake, and its uptake held steady at the second cycle while DOTATOC's fell.
Pig dosimetry for human dose planning
In five pigs the tracer left the blood quickly and collected in liver, spine and kidneys, with none seen in the spleen. Scaled to a 70 kg person receiving 5 GBq, the kidneys would get 13.7 Gy, within accepted limits; no metabolites were found.
Why the antagonist binds more
In cells carrying the human receptor, affinity was similar to lutetium dotatate (dissociation constants 0.15 vs 0.08 nM), but the antagonist recognised four times more sites, and the agonist could displace only 30% of it. Most of the antagonist stayed on the surface, while dotatate was taken inside.
Design of the OPS201/OPS202 pair
Describes how JR11 was developed and why it carries DOTA for therapy (OPS201) and NODAGA for gallium-68 imaging (OPS202): the same peptide sequence with different chelators, taken from bench studies into clinical trials.
The most studied antagonist
Reviews preclinical and clinical data on lutetium-177 satoreotide tetraxetan, the most extensively investigated somatostatin receptor antagonist, noting that antagonists bind more receptor sites and stay longer in tumours despite little internalisation.
Dosing Data
Satoreotide tetraxetan has no approved label. It is given by radioactivity, in a nuclear-medicine department, within trials. The rows below are the activities reported in the human studies carded above.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no regulator's label that says in what form Satoreotide Tetraxetan is supplied. It is a radioactive drug: the next part says where it is prepared and given.
Mixing a vial: a worked example
Nothing to mix at home, and no syringe units to work out: Satoreotide Tetraxetan is a radioactive drug, prepared and given in nuclear-medicine departments, and its dose is an amount of radioactivity (MBq or GBq), not a weight.
This page's dosing note: “Satoreotide tetraxetan is labelled in a hospital radiopharmacy and given by radioactivity, often adjusted by dosimetry; no reconstitution maths applies.”
Source: this page's own note in Dosing Data below; the amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label on file says how Satoreotide Tetraxetan is stored. It is a radioactive drug held by the nuclear-medicine department that prepares and gives it (see the part above); the home rules for a mixed vial in the mixing guide do not apply to it.
How it is taken
As it was given in human studies: Intravenous (Per cycle; Lutetium-177 satoreotide tetraxetan, phase 1/2 part A).
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 127 hours, median terminal blood half-life of lutetium-177 satoreotide tetraxetan after the first cycle (PMID 38528164). After about five half-lives almost none is left.
How long the doses were given: Lutetium-177 satoreotide tetraxetan, phase 1/2 part A: 3 cycles; Lutetium-177 satoreotide tetraxetan, phase 1/2 part B: 1-5 cycles; Lutetium-177 DOTA-JR11 after DOTATOC (meningioma): 2-3 cycles.
When effects appear: unknown; no source on this page gives a time to effect for Satoreotide Tetraxetan. Results reported in the studies are under Published Research.
Source: half-life: PMID 38528164; 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: Low lymphocyte, platelet and neutrophil counts, the main toxicity; grade 3 or worse treatment-related events in 42.5% of 40 patients; Grade 4 blood toxicity in four of seven patients after a second high-activity cycle in the first phase 1 trial; Two treatment-related myeloid neoplasms in the phase 1/2 study; No grade 3 or 4 kidney toxicity in the phase 1/2 study. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Satoreotide Tetraxetan. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the human studies above”).
Interactions
Unknown: a PubMed search for human interaction studies of Satoreotide Tetraxetan (reviewed 2026-10-28) 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 Satoreotide Tetraxetan 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 Satoreotide Tetraxetan's expected mass, 1,689.3 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: Drugs@FDA and the EMA medicines list hold no record (searched October 28, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the human studies above.
Contraindications & Cautions
No approved label exists, so there are no official contraindications. Points from the studies:
Legal Status
Satoreotide tetraxetan is investigational in every jurisdiction checked.
Frequently Asked Questions
?What is satoreotide tetraxetan?
The somatostatin receptor antagonist peptide JR11 with a DOTA chelator, usually labelled with lutetium-177 for treatment. It is also called DOTA-JR11 and OPS201.
?How is it different from lutetium-177 dotatate?
Dotatate switches the receptor on and is taken into the cell. This drug blocks the receptor and stays on the surface, but binds more sites, so tumours received higher doses in comparisons. Marrow doses were higher too.
?Does it work?
In a 40-patient phase 1/2 study, 94.7% had disease control and 21.1% a response. There is no randomised comparison with standard treatment yet.
?What are the main side effects?
Falls in blood counts, sometimes severe, and two cases of treatment-related myeloid neoplasm in the phase 1/2 study.
?Is it approved?
No. It is given only within trials or compassionate-use programmes in nuclear-medicine departments.
References
- [other] PubChem CID 24894654, Satoreotide Tetraxetan: formula C74H98ClN19O21S2, molecular weight 1689.3. Read October 28, 2026. https://pubchem.ncbi.nlm.nih.gov/compound/24894654
- [registry] ClinicalTrials.gov API v2, read October 28, 2026: NCT04997317 (phase 1/2, meningioma, recruiting); NCT02592707 and NCT03773133 (phase 1/2, neuroendocrine tumours, terminated).
- [other] ChEMBL CHEMBL4297531, satoreotide tetraxetan (synonyms include DOTA-JR-11): maximum clinical phase 2 in the ChEMBL molecule record, read October 2, 2026 (the Registry's ChEMBL harvest). https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL4297531/
- [clinical-trial] Wild D, et al. "A phase I/II study of the safety and efficacy of [(177)Lu]Lu-satoreotide tetraxetan in advanced somatostatin receptor-positive neuroendocrine tumours." Eur J Nucl Med Mol Imaging, 2023;51(1):183-195. PMID: 37721581.
- [clinical-trial] Schürrle SB, et al. "Dosimetry and pharmacokinetics of [(177)Lu]Lu-satoreotide tetraxetan in patients with progressive neuroendocrine tumours." Eur J Nucl Med Mol Imaging, 2024;51(8):2428-2441. PMID: 38528164.
- [clinical-trial] Reidy-Lagunes D, et al. "Phase I Trial of Well-Differentiated Neuroendocrine Tumors (NETs) with Radiolabeled Somatostatin Antagonist (177)Lu-Satoreotide Tetraxetan." Clin Cancer Res, 2019;25(23):6939-6947. PMID: 31439583.
- [pubmed] Wild D, et al. "Comparison of somatostatin receptor agonist and antagonist for peptide receptor radionuclide therapy: a pilot study." J Nucl Med, 2014;55(8):1248-52. PMID: 24963127.
- [clinical-trial] Eigler C, et al. "Radiolabeled Somatostatin Receptor Antagonist Versus Agonist for Peptide Receptor Radionuclide Therapy in Patients with Therapy-Resistant Meningioma: PROMENADE Phase 0 Study." J Nucl Med, 2024;65(4):573-579. PMID: 38423782.
- [pubmed] Mushaweh A, et al. "Increased progression free survival with radiolabelled somatostatin receptor antagonist versus standard peptide receptor radionuclide therapy in patients with somatostatin receptor positive tumours." Eur J Nucl Med Mol Imaging, 2026;53(9):5219-5229. PMID: 41874627.
- [pubmed] Schmidt F, et al. "Radiolabelled somatostatin receptor antagonist versus agonist for peptide receptor radionuclide therapy in patients with metastatic pheochromocytoma or paraganglioma: a retrospective pilot study." Eur J Nucl Med Mol Imaging, 2026. PMID: 42581163.
- [clinical-trial] Krebs S, et al. "Comparison of (68)Ga-DOTA-JR11 PET/CT with dosimetric (177)Lu-satoreotide tetraxetan ((177)Lu-DOTA-JR11) SPECT/CT in patients with metastatic neuroendocrine tumors undergoing peptide receptor radionuclide therapy." Eur J Nucl Med Mol Imaging, 2020;47(13):3047-3057. PMID: 32378020.
- [clinical-trial] Krebs S, et al. "Biodistribution and radiation dose estimates for (68)Ga-DOTA-JR11 in patients with metastatic neuroendocrine tumors." Eur J Nucl Med Mol Imaging, 2019;46(3):677-685. PMID: 30374529.
- [pubmed] Zhu W, et al. "Head-to-Head Comparison of (68)Ga-DOTA-JR11 and (68)Ga-DOTATATE PET/CT in Patients with Metastatic, Well-Differentiated Neuroendocrine Tumors: A Prospective Study." J Nucl Med, 2020;61(6):897-903. PMID: 31676731.
- [pubmed] Wang P, et al. "The usefulness of [(68) Ga]Ga-DOTA-JR11 PET/CT in patients with meningioma: comparison with MRI." Eur J Nucl Med Mol Imaging, 2023;51(1):218-225. PMID: 37682301.
- [pubmed] Hou G, et al. "Head-to-Head Comparison of (68)Ga-DOTA-TATE and (68)Ga-DOTA-JR11 PET/CT in Patients With Tumor-Induced Osteomalacia: A Prospective Study." Front Oncol, 2022;12:811209. PMID: 35280786.
- [pubmed] Nicolas GP, et al. "Biodistribution, Pharmacokinetics, and Dosimetry of (177)Lu-, (90)Y-, and (111)In-Labeled Somatostatin Receptor Antagonist OPS201 in Comparison to the Agonist (177)Lu-DOTATATE: The Mass Effect." J Nucl Med, 2017;58(9):1435-1441. PMID: 28450554.
- [pubmed] Plas P, et al. "Comparison of the Anti-Tumour Activity of the Somatostatin Receptor (SST) Antagonist [(177)Lu]Lu-Satoreotide Tetraxetan and the Agonist [(177)Lu]Lu-DOTA-TATE in Mice Bearing AR42J SST(2)-Positive Tumours." Pharmaceuticals (Basel), 2022;15(9). PMID: 36145306.
- [pubmed] Dalm SU, et al. "Comparison of the Therapeutic Response to Treatment with a 177Lu-Labeled Somatostatin Receptor Agonist and Antagonist in Preclinical Models." J Nucl Med, 2016;57(2):260-5. PMID: 26514177.
- [pubmed] Albrecht J, et al. "Multimodal Imaging of 2-Cycle PRRT with (177)Lu-DOTA-JR11 and (177)Lu-DOTATOC in an Orthotopic Neuroendocrine Xenograft Tumor Mouse Model." J Nucl Med, 2021;62(3):393-398. PMID: 32859703.
- [pubmed] Beykan S, et al. "(177)Lu-OPS201 targeting somatostatin receptors: in vivo biodistribution and dosimetry in a pig model." EJNMMI Res, 2016;6(1):50. PMID: 27294582.
- [pubmed] Mansi R, et al. "Distinct In Vitro Binding Profile of the Somatostatin Receptor Subtype 2 Antagonist [(177)Lu]Lu-OPS201 Compared to the Agonist [(177)Lu]Lu-DOTA-TATE." Pharmaceuticals (Basel), 2021;14(12). PMID: 34959665.
- [review] Mansi R, et al. "Design and development of the theranostic pair (177) Lu-OPS201/(68) Ga-OPS202 for targeting somatostatin receptor expressing tumors." J Labelled Comp Radiopharm, 2019;62(10):635-645. PMID: 31112618.
- [review] Shekhda KM, et al. "The Role of [177Lu] Lu-Satoreotide Tetraxetan in Somatostatin Receptor-Positive Neuroendocrine Tumors." Semin Nucl Med, 2025. PMID: 40796453.
- [pubmed] Jafari E, et al. "From Bench to Bedside: A Critical Appraisal of Somatostatin Receptor Antagonists in the Theranostic Management of Neuroendocrine Neoplasms." J Nucl Med, 2026. PMID: 42754346.
Sources & Citations
Studies were read from their PubMed records on October 29, 2026. Regulatory status comes from Drugs@FDA and the EMA medicines list (searched October 28, 2026) and trial listings from ClinicalTrials.gov (October 29, 2026). Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.