Prokineticin 1 (EG-VEGF)
An endogenous angiogenic peptide that builds blood vessels selectively in reproductive and endocrine tissue — central to the placenta, and a pregnancy biomarker. A research peptide, not a drug
Prokineticin 1 (PROK1), far better known as EG-VEGF — endocrine-gland-derived vascular endothelial growth factor — is the sister of prokineticin 2 and a member of the AVIT peptide family. Where the famous VEGF grows blood vessels throughout the body, EG-VEGF does it selectively, mainly in hormone-making (steroidogenic) and reproductive tissues such as the ovary, testis and especially the placenta. It is a central player in early pregnancy: it helps build the corpus luteum, supports the embryo implanting, and drives the blood-vessel growth that a developing placenta needs. Because of this, its level in a pregnant woman’s blood is studied as a warning sign — abnormal EG-VEGF tracks with preeclampsia and predicts spontaneous preterm birth. It also acts on immune cells. EG-VEGF is an endogenous peptide studied as a research tool and a biomarker; it is not an approved medicine and has not been given to people as a treatment.
No established human dose Details ↓
Recommended Dosing
No established human dose
Prokineticin 1 / EG-VEGF is an endogenous human peptide that has never been given to people as a treatment. The human evidence is blood levels (a biomarker of pregnancy complications) and tissue studies, not administration; the interventional work is in animals and cells — and because too much EG-VEGF harms a pregnancy, there is no case for giving it.
Work out syringe units → · New to syringes? · All dosing data ↓ · Dose and vial tracker · Is this vial OK?
What is it?
Prokineticin 1 and prokineticin 2 are the two members of the AVIT peptide family in mammals. Prokineticin 1 was discovered a second time, and named again, by vascular biologists who were looking for a growth factor that builds blood vessels only in certain tissues: they called it EG-VEGF, endocrine-gland-derived vascular endothelial growth factor. Both names describe the same ~86-amino-acid peptide, held in shape by five disulfide bridges, which signals through the receptors PROKR1 and PROKR2.
What makes EG-VEGF distinctive is that its angiogenic power is tissue-selective. Classical VEGF acts on blood-vessel cells almost everywhere; EG-VEGF acts mainly in steroid-hormone-making and reproductive tissues — the ovary, testis, adrenal and, above all, the placenta. In the ovary’s corpus luteum it works as a growth and survival factor for the vessel cells, and it interacts with classical VEGF, the two being reciprocally regulated.
Its headline role is in pregnancy. In the lining of the womb and the early placenta, EG-VEGF is switched on as the embryo implants, and PROK1–PROKR1 signalling drives the blood-vessel growth, cell adhesion and invasion that implantation and placentation require. The same signalling has been mapped in detail in animal and cell models, and EG-VEGF production in the womb lining is itself turned up by insulin — a possible link between insulin resistance (as in obesity or polycystic ovary syndrome) and placenta-related pregnancy problems.
That central placental role makes EG-VEGF a biomarker. Its blood level is abnormal in several pregnancy complications — preeclampsia, fetal growth restriction, recurrent pregnancy loss and preterm birth — and in a prospective study of high-risk women, higher maternal EG-VEGF in the second and third trimesters predicted spontaneous preterm birth with high accuracy. In animals, deliberately keeping EG-VEGF elevated in early gestation reproduces most features of preeclampsia, direct evidence that too much of it is harmful to a pregnancy.
EG-VEGF reaches beyond reproduction. It acts on the immune system — pushing bone-marrow cells and blood monocytes toward an inflammatory, antigen-presenting state — and, like its sister prokineticin 2, it is studied in angiogenesis and cancer. Across these settings the therapeutic interest is in the prokineticin receptors as drug targets, not in giving EG-VEGF.
Prokineticin 1 is an endogenous human peptide and a research and biomarker tool, not a medicine. No published study has given EG-VEGF to people as a treatment — the human evidence is blood levels and tissue — it is approved nowhere, and material sold online as ‘prokineticin 1’ or ‘EG-VEGF’ is an unregulated research chemical. Nothing here is a dose or a therapy; this page records what the published science says about the peptide.
Mechanism of Action
Prokineticin 1 / EG-VEGF is an AVIT-family peptide that works through the prokineticin receptors PROKR1 and PROKR2. It builds blood vessels selectively in reproductive and endocrine tissue, drives implantation and placentation, and acts on immune cells — and too much of it harms a pregnancy.
Tissue-selective angiogenesis (EG-VEGF)
Through PROKR1 and PROKR2, EG-VEGF drives blood-vessel growth selectively in steroid-making and reproductive tissues — the ovary, placenta and endocrine glands — acting as a growth and survival factor for the vessel cells and interacting with classical VEGF (PMID 16320832).
Implantation and placentation
PROK1–PROKR1 signalling supports embryo implantation and placental development — driving trophoblast angiogenesis, adhesion and invasion (PMID 34215801) — and is itself raised by insulin in the womb lining (PMID 28782224); abnormal levels mark preeclampsia and preterm birth (PMID 37963927).
Immune and disease effects
EG-VEGF also acts on the immune system, pushing monocytes toward an inflammatory state (PMID 15908459), and keeping it elevated in early pregnancy reproduces preeclampsia in mice (PMID 29197014) — so the therapeutic interest is in its receptors, not in giving it.
Published Research
These are studies of prokineticin 1 / EG-VEGF read from their PubMed abstracts on November 6, 2026. They include a human prospective cohort using maternal EG-VEGF to predict preterm birth, a review of its role in the corpus luteum, animal and cell studies of its control of implantation and placentation and its regulation by insulin, its effect on immune (monocyte) cells, and an animal model in which keeping EG-VEGF high produces preeclampsia. Prokineticin 1 has not been given to people as a treatment in any published study; the human evidence is biomarker and tissue work.
Maternal EG-VEGF predicts spontaneous preterm birth
In a prospective multicenter cohort of 200 pregnant women at high risk of placenta-mediated complications, those who went on to have a spontaneous preterm birth had higher serum EG-VEGF at 24, 28 and 32 weeks. At 32 weeks the test reached an area under the curve of about 0.9 with 100% sensitivity for predicting spontaneous preterm birth, supporting serum EG-VEGF as a biomarker in high-risk pregnancies — an observational, predictive study, not a treatment.
EG-VEGF / prokineticin-1 in the corpus luteum
A review of EG-VEGF/prokineticin-1 in the ovary’s corpus luteum. It is made by the luteal steroid-making cells and acts on luteal blood-vessel cells, which carry both receptors (PROKR1 and PROKR2), as a growth and survival factor — raising their proliferation and protecting them from apoptosis. EG-VEGF and classical VEGF are reciprocally regulated, suggesting EG-VEGF has roles in the ovary beyond angiogenesis.
PROK1-PROKR1 promotes implantation and placentation
In the pig, prokineticin 1 was elevated in trophoblast during implantation and early placentation, and PROK1–PROKR1 signalling switched on genes for angiogenesis, immune response, cell adhesion, invasion and proliferation, and increased trophoblast proliferation and adhesion through PI3K/AKT/mTOR, MAPK and cAMP pathways. The study concluded PROK1 plays a pleiotropic role in trophoblast function during implantation and placentation (a preclinical result).
Insulin up-regulates PROK1 in human endometrium
In decidualizing human endometrial stromal cells from healthy women, insulin dose-dependently raised prokineticin 1 (a hypoxia-regulated angiogenic factor linked to recurrent pregnancy loss, preeclampsia, growth restriction and preterm birth), acting through HIF1α and the PI3K pathway. PROK1 in turn inhibited the migration of endometrial cells and the migration/invasion of trophoblasts — suggesting high insulin could contribute to placenta-related complications via PROK1.
PK1/EG-VEGF activates monocytes
Beyond blood vessels, PK1/EG-VEGF was shown to act on immune cells: it drove mouse and human bone-marrow cells to differentiate into the monocyte/macrophage lineage and changed human blood monocytes — raising pro-inflammatory cytokines (IL-12, TNF-α) and lowering IL-10 — priming a T-helper-1-type inflammatory response. This identified macrophages as a cellular target of prokineticin 1.
Keeping EG-VEGF high models preeclampsia
A protocol in which EG-VEGF production was maintained in pregnant mice over the first ~11.5 days of gestation caused pregnancy-induced hypertension, reproducing most hallmarks of preeclampsia. The model gave direct in-vivo evidence that excess EG-VEGF in early pregnancy is harmful and contributes to the disease — a preclinical, mechanistic result.
No Established Human Dose
Prokineticin 1 / EG-VEGF is an endogenous human peptide that has never been given to people as a treatment. The human evidence is blood levels (a biomarker of pregnancy complications) and tissue studies, not administration; the interventional work is in animals and cells — and because too much EG-VEGF harms a pregnancy, there is no case for giving it. No regulator has approved any dose, and the experimental amounts used in animals and cells do not carry over to people, so no amount is printed here.
What this rests on: PMID 37963927, PMID 34215801, PMID 29197014.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, 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 Prokineticin 1 (EG-VEGF) is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Prokineticin 1 (EG-VEGF) has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Prokineticin 1 (EG-VEGF), 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 Prokineticin 1 (EG-VEGF) stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Prokineticin 1 (EG-VEGF). What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
How long it stays in the body: a half-life of not established for humans as a drug; an endogenous circulating peptide. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Prokineticin 1 (EG-VEGF). Results reported in the studies are under Published Research.
Source: half-life: PMID 37963927.
Side effects, and when to stop or get help
From the Side Effects section: No human adverse-event data exist: no published study has administered prokineticin 1 to people; High maternal EG-VEGF is associated with pregnancy complications — preeclampsia, growth restriction and preterm birth (PMIDs 37963927, 28782224); In animals, keeping EG-VEGF elevated in early pregnancy reproduces preeclampsia (PMID 29197014), so raising it would be expected to harm a pregnancy; Material sold online as ‘prokineticin 1’ or ‘EG-VEGF’ is an unregulated research chemical of unverified content. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Prokineticin 1 (EG-VEGF). Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Prokineticin 1 is an endogenous peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status”).
Interactions
Unknown: a PubMed search for human interaction studies of Prokineticin 1 (EG-VEGF) (reviewed 2026-11-06) 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 Prokineticin 1 (EG-VEGF) 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. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a drug: Drugs@FDA and the openFDA label endpoint hold no record, and FDA GSRS and ChEMBL hold no substance record for prokineticin 1 / EG-VEGF (searched November 6, 2026)). Sport: Not on the 2026 List.
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
Prokineticin 1 is an endogenous peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status.
Contraindications & Cautions
Prokineticin 1 has no approved use and no label. These points reflect its endogenous, research status.
Legal Status
Prokineticin 1 (EG-VEGF) is an endogenous human peptide studied as a research compound and biomarker; it is not a drug and is not approved in any country.
Frequently Asked Questions
?What is prokineticin 1?
An endogenous human peptide, better known as EG-VEGF (endocrine-gland-derived VEGF). It is an AVIT-family peptide, the sister of prokineticin 2, that signals through the receptors PROKR1 and PROKR2 and builds blood vessels selectively in reproductive and endocrine tissue.
?What does it do?
It drives tissue-selective angiogenesis and is central to the corpus luteum, embryo implantation and placentation (PMIDs 16320832, 34215801). Its blood level is a biomarker of pregnancy complications such as preeclampsia and preterm birth (PMID 37963927), and it also activates immune cells (PMID 15908459).
?Is it a treatment for anything?
No. Prokineticin 1 is a research peptide and a pregnancy biomarker; its receptors are drug targets. Giving it is not a therapeutic idea — too much EG-VEGF harms a pregnancy (PMID 29197014). No human trial has administered it, and it is approved nowhere.
?Is it approved or available to buy?
No. Prokineticin 1 is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as prokineticin 1 or EG-VEGF is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [mechanism] Raia-Barjat T, et al. "EG-VEGF maternal levels predict spontaneous preterm birth in the second and third trimesters in pregnant women with risk factors for placenta-mediated complications." Sci Rep, 2023;13(1):19921. PMID: 37963927.
- [review] Kisliouk T, et al. "Unique expression and regulatory mechanisms of EG-VEGF/prokineticin-1 and its receptors in the corpus luteum." Ann Anat, 2005;187(5-6):529-37. PMID: 16320832.
- [animal] Goryszewska-Szczurek E, et al. "Prokineticin 1-prokineticin receptor 1 signaling in trophoblast promotes embryo implantation and placenta development." Sci Rep, 2021;11(1):13715. PMID: 34215801.
- [mechanism] Ujvari D, et al. "Prokineticin 1 is up-regulated by insulin in decidualizing human endometrial stromal cells." J Cell Mol Med, 2018;22(1):163-172. PMID: 28782224.
- [mechanism] Dorsch M, et al. "PK1/EG-VEGF induces monocyte differentiation and activation." J Leukoc Biol, 2005;78(2):426-34. PMID: 15908459.
- [animal] Reynaud D, et al. "EG-VEGF Maintenance Over Early Gestation to Develop a Pregnancy-Induced Hypertensive Animal Model." Methods Mol Biol, 2018;1710:317-324. PMID: 29197014.
- [other] UniProt P58294 (PROK1_HUMAN), read November 6, 2026: prokineticin 1, also called EG-VEGF, is the product of the PROK1 gene, a secreted ~86-amino-acid peptide of the AVIT family held by five disulfide bridges; it signals through the G-protein-coupled receptors PROKR1 and PROKR2. https://www.uniprot.org/uniprotkb/P58294/entry
- [other] Prokineticin 1 was identified as endocrine-gland-derived vascular endothelial growth factor (EG-VEGF), a tissue-selective angiogenic factor and one of the two AVIT-family prokineticins (with prokineticin 2 / Bv8) acting on PROKR1 and PROKR2; its reproductive biology is set out in the corpus-luteum review carded on this page (read November 6, 2026).
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 6, 2026: no application and no label record for prokineticin 1 / EG-VEGF. It is an endogenous human peptide, not a registered drug; FDA GSRS and ChEMBL hold no substance record for it.
Sources & Citations
The six studies carded above were read from their PubMed records on November 6, 2026. Identity comes from UniProt (P58294, gene PROK1); prokineticin 1’s identity as EG-VEGF, its PROKR1/PROKR2 receptors and its placental role are from the review and studies carded here; the absence of US approval and of a drug substance record from Drugs@FDA, openFDA, FDA GSRS and ChEMBL was checked the same day. 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.