Veldoreotide
A backbone-cyclic somatostatin analogue built to suppress growth hormone while sparing insulin, whose acromegaly trials were never published
Veldoreotide (DG3173, somatoprim, PTR-3173, COR-005) is a small cyclic peptide that imitates somatostatin at receptor subtypes 2, 4 and 5. Over twenty years it passed through Peptor, Aspireo and Strongbridge and reached phase 2 trials in acromegaly, but no results were posted or published. What is in print is laboratory and animal work, plus human pituitary tissue studied in a dish, showing it lowers growth hormone with little effect on insulin.
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What is it?
Veldoreotide is a small synthetic peptide built to copy the way the natural hormone somatostatin shuts down the release of growth hormone. Somatostatin acts through five receptor subtypes, numbered 1 to 5; the analogues already in the clinic, octreotide and lanreotide, work mainly through subtype 2. Veldoreotide was designed with a different reach: it binds subtypes 2, 4 and 5. It carries four development codes from four owners over more than twenty years, which is why the literature is scattered. Peptor in Israel first described it as PTR-3173; Develogen and then Aspireo Pharmaceuticals developed it as DG3173, trade-named somatoprim; and in July 2015 Cortendo, later Strongbridge Biopharma, bought it from Aspireo and renamed it COR-005.
Chemically it is a backbone-cyclic heptapeptide. A 2002 paper gives its ring as c(GABA-Phe-Trp-(D)Trp-Lys-Thr-Phe-GlyC3-NH2), and the public chemistry databases list its formula as C60H74N12O10 and its weight as about 1,123. The cyclic backbone and the mirror-image tryptophan make it resistant to the enzymes that would otherwise chop a peptide apart in the blood, which is what the early work meant by calling it long-acting. ChEMBL files it at a highest clinical phase of 2.
The reason a company would want a somatostatin analogue that reaches subtype 4 and spares insulin is specific to acromegaly. In that disease a pituitary tumour pours out growth hormone; the standard analogues suppress it in about half of patients, but because subtype 5 and subtype 2 also sit on the insulin-making cells of the pancreas, they blunt insulin release and can push blood sugar up. The animal and tissue studies below report that veldoreotide suppresses growth hormone while leaving insulin largely alone, and that it works on some tumours that do not respond to octreotide. That was the case made for testing it in people.
What never followed was a published clinical result. ClinicalTrials.gov lists five Aspireo trials: three phase 1 studies in healthy adults and two short phase 2 studies in untreated acromegaly that measured growth hormone against octreotide. All are marked completed, none posted results to the registry, and no journal paper reporting any of them appears in PubMed. After the 2015 acquisition the drug was folded into a pipeline alongside two other Cortendo compounds, and no later trial under any of its names has reported. So everything on this page about the molecule itself comes from the laboratory bench, from animals, and from pieces of human pituitary tissue studied in a dish.
Because the clinical file is empty, there is no established human dose and no published safety record for veldoreotide in patients. It is approved in no country and is not a marketed medicine. The pages for octreotide, lanreotide and pasireotide carry the human evidence for the somatostatin-analogue class; this page is confined to what has actually been published about veldoreotide.
At a Glance
Every value in this table is printed from the Grey Peptides dataset, the same record the compound explorer and comparison tool read, so the three can never disagree.
Mechanism of Action
Veldoreotide copies somatostatin, the hormone that tells the pituitary to stop releasing growth hormone. Its particular feature is which of the five somatostatin receptors it switches on, and which it leaves alone.
Activates receptor subtypes 2, 4 and 5
Veldoreotide is a full agonist at somatostatin receptor subtypes 2, 4 and 5 (PMID 34685446). Subtype 2 is the main brake on growth-hormone release that octreotide uses; the reach to subtype 4, which the common analogues barely touch, is what sets this molecule apart.
Suppresses growth hormone
In rats it suppressed growth hormone about a thousandfold more readily than glucagon (PMID 11145612), and in human pituitary and tumour cells it cut growth-hormone release as deeply as octreotide, including in some octreotide-resistant tumours (PMIDs 15636423, 22065857).
Spares insulin
The older analogues also quiet the insulin-making cells of the pancreas, which can raise blood sugar. In rats veldoreotide was more than ten thousand times weaker at blocking insulin than growth hormone (PMID 11145612), the selectivity its developers pointed to for patients with diabetes.
A cyclic peptide that resists breakdown
Its backbone-cyclic ring and mirror-image tryptophan make it hard for blood enzymes to cut, which is what the early work meant by long-acting (PMIDs 11145612, 11931620). None of this has been confirmed by published pharmacokinetics in people.
Published Research
The ten studies below are the published work on veldoreotide itself, read from their PubMed abstracts in November 2026: one discovery paper in rats and cells, two on human pituitary tissue in culture, three on which receptors it activates, one on its synthesis, one in diabetic mice, and two acromegaly reviews that name it. There is no human card because no clinical trial of the drug has been published; its five registered trials are described under Legal status. Findings in these papers about octreotide, pasireotide or other analogues belong to those drugs.
The discovery paper: growth hormone down, insulin untouched in rats
Peptor's team screened libraries of backbone-cyclic peptides against each of the five cloned human somatostatin receptors and picked out one, coded PTR-3173, that bound subtypes 2, 4 and 5 with nanomolar strength and resisted enzyme breakdown. In the human carcinoid cell line BON-1 it blocked the second-messenger cyclic AMP as well as octreotide did. The striking result was in rats: the peptide was roughly a thousand times better at suppressing growth hormone than glucagon, and more than ten thousand times better than it was at suppressing insulin. The authors read that gap as the selectivity a growth-hormone-lowering drug would want, with little of the blood-sugar penalty the older analogues carry.
Human fetal pituitary and tumour cells in a dish
Israeli researchers added PTR-3173, here called somatoprim, to cultures of human fetal pituitary tissue and of cells taken from surgically removed growth-hormone-secreting adenomas. It cut growth hormone release from the fetal pituitaries by just over half at 10 nanomolar, matching octreotide, and reduced it by about a third in the adenoma cultures. Thyroid-stimulating hormone was only mildly affected and ACTH not at all. Across eight tumours the two drugs traded places: octreotide won on two, PTR-3173 on three, and three responded to neither. The authors concluded it was a potent suppressor of human growth hormone worth taking forward in acromegaly.
Working where octreotide fails
A Berlin group treated cultures from 27 human growth-hormone-secreting pituitary adenomas with DG3173 or octreotide and counted a response as growth hormone falling below 80 percent of baseline. DG3173 suppressed hormone in more tumours than octreotide did, ten of 21 against five of 21, and it worked in about a third of the tumours that octreotide could not touch. Where both drugs worked, the depth of suppression was similar. The authors tied octreotide's failures to low levels of subtype-2 receptor on the tumour cells and argued that DG3173's extra reach to subtypes 4 and 5, together with its weak effect on insulin, could make it a useful alternative. This was cultured tumour tissue, not a trial in patients.
Reading which receptors it actually switches on
Jena pharmacologists built a reporter that lights up only when a somatostatin receptor is truly activated, by moving the key phosphorylation tag of subtype 2 onto the other subtypes and detecting it with specific antibodies. Measured this way, somatoprim (DG3173) was a full activator of subtype 2, as octreotide was, but unlike octreotide it was also a strong activator of subtype 5. The work was mainly a demonstration of the method; it placed veldoreotide's activation profile between octreotide's narrow one and pasireotide's broad one.
A full agonist at the elusive subtype 4
A later Jena study focused on receptor subtype 4, which the common analogues barely touch. In kidney cells engineered to carry single receptor subtypes, veldoreotide switched on subtype 4 almost completely while octreotide and pasireotide managed only a fraction of that effect. In the human BON-1 cell line it activated subtypes 2, 4 and 5 with high potency, cut secretion of the tumour marker chromogranin A, and slowed cell growth most strongly through subtype 4. The authors classed veldoreotide as a full agonist at subtypes 2, 4 and 5, and noted interest in subtype 4 for pain as well as for tumour biology.
Rebuilding the ring to steer receptor selectivity
Chemists at the Hebrew University took PTR-3173 as a template and made a set of analogues in which the closing bridge of the ring was swapped from a lactam to a sulfur-containing link, using a new on-resin method. The variants kept the metabolic toughness of the parent but shifted which receptors they preferred: a disulfide bridge sharpened binding to subtypes 2 and 5 while weakening the grip on subtype 4 that defines veldoreotide. The lesson was that ring chemistry, size and position tune a somatostatin analogue's receptor profile, which is the dial the whole programme was built around.
A new way to close the ring
Academic and industry chemists published a light-driven reaction that joins a peptide into a ring by removing a carboxyl group, and tolerates unusual amino acids and ring sizes. To show it could make a real drug candidate they used it to synthesise COR-005, naming veldoreotide as a somatostatin analogue then in clinical trials. The paper is about the synthetic method rather than the drug's biology, but it is the clearest published confirmation of the molecule's cyclic structure.
Protecting the kidney in diabetic mice
Because growth hormone and the growth factor it drives, IGF-1, are tied to the early kidney damage of diabetes, an Israeli group gave PTR-3173 to non-obese diabetic mice for three weeks after diabetes set in. Treated mice had lower growth hormone, less enlargement of the kidney and its filtering units, less protein leaking into the urine, and no build-up of IGF-1 in the kidney. The authors read this as evidence that dialling down growth hormone with the analogue could blunt the start of diabetic kidney disease. This was a mouse study, in a condition far from the acromegaly the drug was built for.
Placed among new acromegaly agents
A review of drugs in development for acromegaly groups DG3173 with oral octreotide capsules, the long-acting depot CAM2029 and an antisense drug against the growth-hormone receptor. It describes DG3173 as a pan-selective analogue that had reached phase 1 and phase 2 and had shown it could suppress growth hormone with a favourable safety profile, while cautioning that these investigational agents still had to find their place beside the approved drugs.
Why a broader receptor reach was wanted
A review of newer somatostatin receptor ligands for acromegaly presents DG3173 (somatoprim) as an analogue that appears more selective for suppressing growth hormone, which the authors suggest could be an advantage in patients who also have high blood sugar or diabetes. It sets the molecule beside new formulations of octreotide and the broader-spectrum pasireotide, and notes that whether such features help patients in practice remained to be shown.
Side Effects & Contraindications
Reported Side Effects
No safety data for veldoreotide in people have been published. Its phase 1 and phase 2 trials recorded safety as an outcome, but none posted results or produced a paper.
Contraindications & Cautions
There is no label, so there are no official contraindications. The molecule is not an available medicine.
Legal Status
Veldoreotide is an investigational drug that has never been approved anywhere.
Frequently Asked Questions
?What is veldoreotide?
A small synthetic cyclic peptide that imitates the hormone somatostatin at receptor subtypes 2, 4 and 5, built to lower growth hormone. It has had four names over its life: PTR-3173, DG3173, somatoprim and COR-005. It was studied mainly for acromegaly.
?Did it work in its trials?
Nobody outside the sponsors can say. Aspireo Pharmaceuticals registered three phase 1 trials in healthy adults and two phase 2 trials in acromegaly, all completed, and none posted results on ClinicalTrials.gov or appeared as a paper in PubMed.
?How is it different from octreotide?
Octreotide works mainly through somatostatin receptor subtype 2. Veldoreotide also reaches subtypes 4 and 5, and in laboratory studies it suppressed growth hormone with less effect on insulin and worked in some tumours octreotide could not touch (PMIDs 22065857, 34685446). Whether that matters to patients was never published.
?Why does it have so many names?
Because it changed hands. Peptor first described it as PTR-3173, Aspireo developed it as DG3173 under the trade name somatoprim, and Cortendo (later Strongbridge Biopharma) renamed it COR-005 after buying it in 2015. They are all the same molecule.
?Can anyone get it now?
No. It is approved in no country and no trial is recruiting. Anything sold under its names outside a trial has no established identity, purity or dose, and no safety record in people has ever been published.
References
- [pubmed] Afargan M, et al. "Novel long-acting somatostatin analog with endocrine selectivity: potent suppression of growth hormone but not of insulin." Endocrinology, 2001;142(1):477-86. PMID: 11145612.
- [pubmed] Shimon I, et al. "PTR-3173 (somatoprim), a novel somatostatin analog with affinity for somatostatin receptors 2, 4 and 5 is a potent inhibitor of human GH secretion." J Endocrinol Invest, 2004;27(8):721-7. PMID: 15636423.
- [pubmed] Plöckinger U, et al. "DG3173 (somatoprim), a unique somatostatin receptor subtypes 2-, 4- and 5-selective analogue, effectively reduces GH secretion in human GH-secreting pituitary adenomas even in Octreotide non-responsive tumours." Eur J Endocrinol, 2012;166(2):223-34. PMID: 22065857.
- [pubmed] Kliewer A, et al. "A transplantable phosphorylation probe for direct assessment of G protein-coupled receptor activation." PLoS One, 2012;7(6):e39458. PMID: 22745760.
- [pubmed] Dasgupta P, et al. "Pharmacological Characterization of Veldoreotide as a Somatostatin Receptor 4 Agonist." Life (Basel), 2021;11(10). PMID: 34685446.
- [pubmed] Gazal S, et al. "Human somatostatin receptor specificity of backbone-cyclic analogues containing novel sulfur building units." J Med Chem, 2002;45(8):1665-71. PMID: 11931620.
- [pubmed] McCarver SJ, et al. "Decarboxylative Peptide Macrocyclization through Photoredox Catalysis." Angew Chem Int Ed Engl, 2017;56(3):728-732. PMID: 27860140.
- [pubmed] Landau D, et al. "A novel somatostatin analogue prevents early renal complications in the nonobese diabetic mouse." Kidney Int, 2001;60(2):505-12. PMID: 11473633.
- [pubmed] Melmed S. "New therapeutic agents for acromegaly." Nat Rev Endocrinol, 2016;12(2):90-8. PMID: 26610414.
- [pubmed] Paragliola RM, et al. "Novel Somatostatin Receptor Ligands Therapies for Acromegaly." Front Endocrinol (Lausanne), 2018;9:78. PMID: 29563895.
- [pubmed] Cuevas-Ramos D, et al. "Somatostatin receptor ligands and resistance to treatment in pituitary adenomas." J Mol Endocrinol, 2014;52(3):R223-40. PMID: 24647046.
- [pubmed] Störmann S, et al. "Emerging drugs for acromegaly." Expert Opin Emerg Drugs, 2014;19(1):79-97. PMID: 24400774.
- [pubmed] Segev Y, et al. "Comparison between somatostatin analogues and ACE inhibitor in the NOD mouse model of diabetic kidney disease." Nephrol Dial Transplant, 2004;19(12):3021-8. PMID: 15494355.
- [pubmed] Rubello D, et al. "[New perspectives in diagnosis and therapy of endocrine gastroenteropancreatic (GEP) tumors with somatostatin analogues]." Minerva Endocrinol, 2003;28(4):259-96. PMID: 14752399.
- [registry] ClinicalTrials.gov API v2, read November 5, 2026: Aspireo Pharmaceuticals sponsors five DG3173 records, all completed with no results posted. NCT02217488 (single ascending dose, 72 healthy adults, 2008); NCT02217826 (single-dose pharmacodynamics and pharmacokinetics against octreotide and saline, 8 healthy adults); NCT02217839 (multiple ascending dose against octreotide, 42 healthy adults); NCT02235987 (phase 2, single ascending doses of DG3173 against 300 ug octreotide on growth hormone in 20 untreated people with acromegaly, 2012); NCT02217800 (phase 2, subcutaneous infusions of three DG3173 doses against octreotide and saline in 8 untreated people with acromegaly, 2013-2014). A separate phase 1 record, NCT04138342, studies quantum dots coated with veldoreotide for breast-cancer imaging (Al-Azhar University), a different, conjugated product. https://clinicaltrials.gov/study/NCT02235987
- [manufacturer] Cortendo AB press release, July 2, 2015: Cortendo (later Strongbridge Biopharma) acquired Somatoprim (DG3173), renamed COR-005, from Aspireo Pharmaceuticals for about USD 30 million in Cortendo equity, calling it a next-generation somatostatin analogue investigated for acromegaly with possible use in Cushing's syndrome and neuroendocrine tumours; it cited three phase 1 and two phase 2 single-ascending-dose acromegaly trials, with no phase 3 program named. https://news.cision.com/strongbridge-biopharma-plc/r/cortendo-provides-2015-half-year-update-on-corporate-progress,c9800427
- [other] US FDA substance registry, substance VELDOREOTIDE (UNII 1Z83587HBN), read November 5, 2026: molecular formula C60H74N12O10; synonyms Somatoprim and Veldoreotide [INN], [USAN]; codes COR-005, DG3173, DG-3173, PTR 3173, PTR-3173; CAS 252845-37-7, INN 10521, USAN DE-59. The acetate salt is UNII 9F2286627L. https://drugs.ncats.io/substance/1Z83587HBN
- [other] ChEMBL molecule CHEMBL3989911 (VELDOREOTIDE), read November 5, 2026: molecule type Protein, molecular formula C60H74N12O10, molecular weight 1123.33; synonyms Veldoreotide (INN, USAN), Somatoprim, and research codes COR-005, DG-3173, DG3173, PTR 3173, PTR-3173; highest clinical phase recorded 2. https://www.ebi.ac.uk/chembl/compound_report_card/CHEMBL3989911/
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 5, 2026: no application and no label record for veldoreotide, somatoprim, DG3173 or COR-005.
Sources & Citations
The ten studies carded above and the four References-only papers were read from their PubMed records in November 2026; together with two papers whose abstracts do not name the molecule, they are what a PubMed search for veldoreotide, DG3173, COR-005 or PTR-3173 returns. The sequence comes from a 2002 synthesis paper (PMID 11931620); formula, weight and codes from FDA's substance registry (UNII 1Z83587HBN) and ChEMBL (CHEMBL3989911); trial details from ClinicalTrials.gov; the acquisition history from Cortendo's July 2, 2015 release; United States status from Drugs@FDA and the openFDA label endpoint, all read November 5, 2026. Grey Peptides sells nothing and links to no vendor.
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