At a glance
What is it—and why does it matter?
Neuropeptide Y is classified as a peptide in this ligand entry (Ligand ID: 1504). Neuropeptide Y acts as a full agonist at the human Y2 receptor, with binding affinity reported as pKi 9.3 - 9.5 (higher pKi indicates higher affinity). The abstract reports that genetic whole-body deletion of NPY (NPY-KO) in rats lessened fibrotic remodeling and EndMT, improved cardiac function, and decreased infarct size after MI. A stated limitation for neuropeptide-based imaging probes is rapid degradation/clearance, summarized as a half-life under 30 minutes for most neuropeptides.
Sources for this introduction: [1] [2] [3] [4]
This published profile is a reference in progress. Findings retain their source context; missing topics are marked below.
What is it?
A molecule, not a product name.
Identity
The work reports the design and evaluation of two fluorescent cyclic thioamide peptides, HAP1 and HAP1-RS33, positioned as Y2R-specific agonists and imaging agents.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Herein, we designed and evaluated the first fluorescent cyclic thioamide peptides (HAP1 and HAP1-RS33) as specific agonists and imaging agents of the Y2R.”
Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging. · Abstract
pubmed:42291135:0db6369cdd5a:0db6369cdd5a
Identity
Neuropeptide Y is classified as a peptide in this ligand entry (Ligand ID: 1504).
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Name: neuropeptide Y Ligand ID: 1504 Type: Peptide”
neuropeptide Y · Identity and approval
iuphar-ligand:1504:d592098de433:d592098de433
How does it work?
Target, response, and disposition.
Mechanism
Designing peptide agents as Y2R agonists is stated as a strategy to drive receptor-mediated endocytosis (internalization), supporting their use as imaging probes.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“To develop an effective imaging probe for glioblastomas, peptide-based agents can be designed as Y2R agonists to be internalized by receptor-mediated endocytosis.”
Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging. · Abstract
pubmed:42291135:0db6369cdd5a:0db6369cdd5a
Mechanism
In this work, neuropeptide Y is listed as one of the pancreatic β-cell secretory granule proteins used as a source to computationally generate hybrid insulin peptide (HIP) candidates.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Next, all possible HIP candidates with 7-9 amino acid residues per fragment were generated from eight pancreatic β-cell secretory granule source proteins, including insulin chains and C-peptide, islet amyloid polypeptide, chromogranin A, neuropeptide Y, and two secretogranins, yielding 1,057,374 candidates.”
A multi-level machine learning pipeline for prediction and prioritization of hybrid insulin peptides in type 1 diabetes. · Abstract
pubmed:42630244:ebec02b8743e:ebec02b8743e
Mechanism
Neuropeptide Y acts as a full agonist at the human Y4 receptor, with binding affinity reported as pKi 8.0.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Ligand: neuropeptide Y Target: Y<sub>4</sub> receptor (Human) Action: Full agonist Primary target: no Affinity: pKi 8.0”
IUPHAR interactions for neuropeptide Y · Interaction 3623
iuphar-interactions:1504:7ba1041b81c9:7ba1041b81c9
Mechanism
Thioamide substitution (O-to-S atom replacement) is presented as a chemical modification intended to improve peptide stability, with proposed utility in therapy and imaging.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Thioamide substitution, a single-atom O-to-S modification, is a promising tool to enhance peptide stability for therapeutic and imaging purposes.”
Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging. · Abstract
pubmed:42291135:0db6369cdd5a:0db6369cdd5a
Mechanism
Y2R (a neuropeptide Y receptor subtype) is reported as highly expressed in human neuroblastoma and glioblastoma cells and is described as stimulating cancer cell growth.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“The neuropeptide Y type 2 receptor (Y2R) is highly expressed in human neuroblastoma and glioblastoma cells, and it has been shown to stimulate cancer cell growth.”
Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging. · Abstract
pubmed:42291135:0db6369cdd5a:0db6369cdd5a
Mechanism
Within the avian gut-brain axis framework, arcuate NPY/AgRP neurons are described as central integrators that combine incoming peripheral information (along with downstream hypothalamic and brainstem circuitry) to shape the balance of orexigenic vs anorexigenic neurochemical output pathways.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“At the central level, we describe how arcuate neuropeptide Y/agouti-related peptide (NPY/AgRP) and pro-opiomelanocortin/cocaine- and amphetamine-regulated transcript (POMC/CART) neurons, downstream hypothalamic nuclei, and brainstem relays integrate these inputs into a dynamic balance between opposing orexigenic and anorexigenic neurochemical effector pathways.”
The gut-brain axis in avian appetite regulation: Integrating peripheral signals with central neurocircuitry. · Abstract
pubmed:42247765:55415aa67692:55415aa67692
Mechanism
Neuropeptide Y is annotated as an antagonist at the human PrRP receptor, with binding affinity reported as pKi 5.4.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Ligand: neuropeptide Y Target: PrRP receptor (Human) Action: Antagonist Primary target: no Affinity: pKi 5.4”
IUPHAR interactions for neuropeptide Y · Interaction 4247
iuphar-interactions:1504:7ba1041b81c9:7ba1041b81c9
Mechanism
Neuropeptide Y acts as a full agonist at the human Y5 receptor, with binding affinity reported as pKi 9.1.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Ligand: neuropeptide Y Target: Y<sub>5</sub> receptor (Human) Action: Full agonist Primary target: no Affinity: pKi 9.1”
IUPHAR interactions for neuropeptide Y · Interaction 3669
iuphar-interactions:1504:7ba1041b81c9:7ba1041b81c9
Mechanism
The abstract reports that fasting-induced H2S activated AMPK in the hypothalamic arcuate nucleus via an S-sulfhydration-dependent mechanism, and this was associated with increased activity of neuropeptide Y (NPY)-positive neurons in a feeding-promoting pathway.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Mechanistically, fasting-induced H2S promoted feeding by activating AMP-activated protein kinase (AMPK) in the hypothalamic arcuate nucleus, a key center for feeding regulation, via an S-sulfhydration-dependent mechanism, which in turn enhanced the activity of neuropeptide Y-positive neurons.”
Disruption of gut bacteria-derived hydrogen sulfide signaling mediates antibacterial-induced acute anorexia. · Abstract
pubmed:42667966:da84a0ae8273:da84a0ae8273
Mechanism
Across both genotypes, NPY-immunoreactive neurons show perisomatic appositions from serotonergic inputs and tyrosine hydroxylase-immunoreactive (catecholaminergic) afferents, consistent with monoaminergic innervation patterns.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“In both genotypes, PV- and NPY-ir neurons possess perisomatic appositions by serotonergic and tyrosine hydroxylase-ir afferents.”
Impact of serotonin transporter deficiency on parvalbumin- and neuropeptide Y-producing neurons of the lateral and basolateral amygdalar nuclei. · Abstract
pubmed:42616085:15ff122df0c9:15ff122df0c9
Mechanism
Neuropeptide Y is annotated as an agonist at the human Y1 receptor, indicating it can activate this receptor subtype in the reported interaction dataset.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Ligand: neuropeptide Y Target: Y<sub>1</sub> receptor (Human) Action: Agonist Primary target: no”
IUPHAR interactions for neuropeptide Y · Interaction 82273
iuphar-interactions:1504:7ba1041b81c9:7ba1041b81c9
Mechanism
Neuropeptide Y is annotated as an agonist at the human Y2 receptor, indicating receptor-activating activity in the reported interaction dataset.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Ligand: neuropeptide Y Target: Y<sub>2</sub> receptor (Human) Action: Agonist Primary target: no”
IUPHAR interactions for neuropeptide Y · Interaction 82275
iuphar-interactions:1504:7ba1041b81c9:7ba1041b81c9
Mechanism
Neuropeptide Y acts as a full agonist at the human Y2 receptor, with binding affinity reported as pKi 9.3 - 9.5 (higher pKi indicates higher affinity).
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Ligand: neuropeptide Y Target: Y<sub>2</sub> receptor (Human) Action: Full agonist Primary target: no Affinity: pKi 9.3 - 9.5”
IUPHAR interactions for neuropeptide Y · Interaction 3590
iuphar-interactions:1504:7ba1041b81c9:7ba1041b81c9
Pharmacokinetics
A stated limitation for neuropeptide-based imaging probes is rapid degradation/clearance, summarized as a half-life under 30 minutes for most neuropeptides.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“However, the short half-life of most neuropeptides (<30 minutes) makes them unsuitable as imaging probes.”
Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging. · Abstract
pubmed:42291135:0db6369cdd5a:0db6369cdd5a
What has been studied?
What the evidence says.
Study findings
The abstract reports pharmacologic antagonism/inhibition (NPY1R antagonist BIBO3304 and JAK2/STAT3 inhibitor WP1066) countered NPY-associated cardiac functional impairment and fibrotic/EndMT-like outcomes in rats.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“NPY1R antagonist (BIBO3304) and JAK2/STAT3 inhibitor (WP1066) alleviated cardiac dysfunction, reduced cardiac fibrosis and mitigated EndMT-like changes in rats after NPY administration.”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
In NPY-expressing tSPNs, repetitive firing gain (the f–I slope) was increased, reflecting increased excitability during repetitive firing.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“NPY+tSPNs had changes in active membrane properties including an increased repetitive firing output gain (↑f-Islope), which modeling attributed to reduced delayed rectifier currents (IK).”
Plasticity in Thoracic Paravertebral Sympathetic Postganglionic Neurons after High Spinal Cord Transection. · Abstract
pubmed:42442958:8502284e3cb2:8502284e3cb2
Study findings
The abstract reports that genetic whole-body deletion of NPY (NPY-KO) in rats lessened fibrotic remodeling and EndMT, improved cardiac function, and decreased infarct size after MI.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Whole-body knock-out NPY (NPY-KO) in rats ameliorated cardiac fibrosis, endothelial mesenchymal transition (EndMT) and cardiac dysfunction and reduced infarct size after myocardial infarction.”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
Cell counting/density quantification indicated a decrease in NPY-immunoreactive neuron number and density within the BLA in serotonin transporter knockout mice.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Quantification of PV- and NPY-ir neurons documents a reduction in numbers and densities of NPY-ir neurons of the BLA in 5-HTT KO mice while PV-ir neuron numbers and densities remain unchanged.”
Impact of serotonin transporter deficiency on parvalbumin- and neuropeptide Y-producing neurons of the lateral and basolateral amygdalar nuclei. · Abstract
pubmed:42616085:15ff122df0c9:15ff122df0c9
Study findings
The abstract states that exogenous NPY treatment in rats increased fibrotic remodeling and EndMT and worsened cardiac function outcomes (without quantitative detail).
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“In contrast, treatment with NPY in rats promoted cardiac fibrosis, EndMT and cardiac dysfunction.”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
In a rat MI context, the abstract reports increased NPY in both circulating serum and fibrotic cardiac tissue.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“NPY levels were found to be elevated in the serum and fibrotic rat heart tissues after myocardial infarction (MI).”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
In a mouse study, acetylated starch was associated with reduced immunofluorescent signals from orexigenic NPY neurons in the arcuate nucleus, consistent with decreased apparent NPY-neuron activity by this readout.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“AS lowered food intake and reduced immunofluorescent signals from orexigenic agouti-related peptide (AgRP) and neuropeptide Y (NPY) neurons in the arcuate nucleus.”
Acetylated starch promotes satiety by inhibiting hypothalamic agouti-related peptide and neuropeptide Y neurons. · Abstract
pubmed:42641527:2385981ab1a6:2385981ab1a6
Study findings
The abstract reports that blocking NPY1R (BIBO3304) or inhibiting JAK2/STAT3 signaling (WP1066) reduced NPY-driven fibroblast activation and EndMT-like phenotypic changes in vitro.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“whereas BIBO3304 and WP1066 inhibited fibroblast activation and EndMT-like changes induced by NPY.”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
Using dual immunolabeling, PV and NPY did not colocalize, indicating distinct PV-positive versus NPY-positive neuronal populations under the conditions studied.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Dual immunolabeling shows no colocalization of PV and NPY.”
Impact of serotonin transporter deficiency on parvalbumin- and neuropeptide Y-producing neurons of the lateral and basolateral amygdalar nuclei. · Abstract
pubmed:42616085:15ff122df0c9:15ff122df0c9
Study findings
NPY-expressing tSPNs showed reduced dendritic length, indicating a morphological change in this neuronal subpopulation.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Dendritic length was reduced, as was measured cell capacitance in neuropeptide Y-expressing (NPY+) tSPNs (putative vasoconstrictors), which represent >40% of tSPNs.”
Plasticity in Thoracic Paravertebral Sympathetic Postganglionic Neurons after High Spinal Cord Transection. · Abstract
pubmed:42442958:8502284e3cb2:8502284e3cb2
Study findings
The abstract states that NPY increases proliferative activity, extracellular matrix (collagen) production, and EndMT in both cardiac fibroblasts and human coronary artery endothelial cells.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Similarly, NPY promoted cell proliferation, collagen production, and EndMT in CFs and HCAECs,”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
The abstract reports that knocking down NPY with siRNA attenuated TGF-β1-driven fibroblast activation and EndMT-related changes in both neonatal rat cardiac fibroblasts and human coronary artery endothelial cells.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Additionally, NPY small interfering RNA (siRNA) in neonatal rat cardiac fibroblasts (CFs) and human coronary artery endothelial cells (HCAECs) reduced fibroblast activation and EndMT in response to TGF-β1 stimulation,”
Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. · Abstract
pubmed:42612877:028dd5c80d77:028dd5c80d77
Study findings
NPY-expressing tSPNs had lower measured cell capacitance, consistent with altered neuronal membrane properties.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Dendritic length was reduced, as was measured cell capacitance in neuropeptide Y-expressing (NPY+) tSPNs (putative vasoconstrictors), which represent >40% of tSPNs.”
Plasticity in Thoracic Paravertebral Sympathetic Postganglionic Neurons after High Spinal Cord Transection. · Abstract
pubmed:42442958:8502284e3cb2:8502284e3cb2
Risks and interactions
Risks, organized for scanning.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
Products and regulatory status
Same ingredient. Different records.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
Administration context
The practical clinical context.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
Additional research & classification gaps
6 archived statements are kept separate from drug-effect findings. Media studies, economic models, methods, and records with unresolved scope are not used as medical-effect evidence.
Inspect contextual research (6)
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
The probe is reported to function as an imaging agent that selectively visualizes neuroblastoma cells expressing Y2R.
Research context only—not evidence of a treatment effect.
- Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging.
Our stabilized cyclized thiopeptide probe showed a significant improvement in half-life from approximately 30 minutes to over 8 hours while maintaining moderate potency and high selectivity for binding with Y2R receptor expressing cells, enabling selective imaging of Y2R-expressing neuroblastoma cells.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Using multiplex fluorescent in situ hybridization in postmortem samples, the investigators quantified NPY mRNA within the CHODL-SST interneuron subtype across DLPFC and caudate, comparing schizophrenia vs unaffected individuals.
Research context only—not evidence of a treatment effect.
- Molecular alterations in chondrolectin-containing somatostatin neurons in schizophrenia differ based on circuit context.
Using multiplex fluorescent in situ hybridization in postmortem tissue from 18 matched pairs of schizophrenia and unaffected comparison individuals, we quantified mRNA levels of CHODL, SST, neuropeptide Y (NPY), and nitric oxide synthase (NOS1) within CHODL-SST neurons in both regions.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
The abstract states that NPY concentration increases during the pathological progression of heart failure.
Research context only—not evidence of a treatment effect.
- Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway.
The level of neuropeptide Y (NPY) is elevated during the pathological progression of heart failure (HF).
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
In this review, neuropeptide Y (NPY) is identified among neuropeptides discussed for neuroprotective roles in acute neurological injury contexts.
Research context only—not evidence of a treatment effect.
- From Self-Assembly to Survival: Neuropeptide Precursor Biology in Neuroprotection.
We further review how key neuroprotective NPs, including α-melanocyte-stimulating hormone (α-MSH), galanin, orexins, neuropeptide Y (NPY), neuropeptide S (NPS), nesfatin-1, and adrenocorticotropic hormone (ACTH)-derived peptides, mitigate acute neuronal injury by modulating microglial activation, inflammatory cytokine production, excitatory-inhibitory balance, and apoptotic pathways.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Proteolytic stability assessment was performed by incubating peptides in mouse serum and using HPLC/MS to map cleavage sites, which is stated to confirm enhanced stability.
Research context only—not evidence of a treatment effect.
- Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging.
High-performance liquid chromatography and mass spectrometry were used to identify cleavage sites by analyzing peptides after incubating in mouse serum, confirming enhanced stability of the peptides.
4 cited sources · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
6 cited passages across 4 source records. 3 publication group(s) lack a resolved study identity.
Neuropeptide-Y (NPY) is described as being involved in pathological processes associated with epileptogenesis.
Research context only—not evidence of a treatment effect.
- The Effect of Respiratory Muscle Performance on Cognitive Functions in Children with Epilepsy: Monitoring with Glymphatic System Activation and Neuropeptides
Neuropeptide-Y (NPY) and neural growth factor (NGF) play a role in different pathological processes seen in epileptogenesis.
- The Role of Hippocampal Interneuron Migration in Neurodevelopmental Disorders: A Systematic Review.
Following screening, we identified 29 articles which met the inclusion/exclusion criteria for the study.
- The Role of Hippocampal Interneuron Migration in Neurodevelopmental Disorders: A Systematic Review.
We adhered to the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines to perform a comprehensive review of the existing research on GABAergic, parvalbumin, somatostatin, cholecystokinin, neuropeptide Y, calbindin, and calretinin interneuron migration in the hippocampus.
- The Role of Hippocampal Interneuron Migration in Neurodevelopmental Disorders: A Systematic Review.
Three blocks of search terms were used to extract 1459 papers from the PubMed, PsycINFO, and Web of Science databases.
- Exercise-induced neuropeptidergic and neurochemical neuroadaptation in stress regulation and emotional disorders.
We discuss exercise-associated adaptations involving dopaminergic, serotonergic, noradrenergic, glutamatergic, GABAergic, endocannabinoid, and opioid-related signaling, together with stress-responsive neuropeptides including corticotropin-releasing hormone, neuropeptide Y, oxytocin, orexin, β-endorphin, and substance P.
- The neuroendocrine network imbalance in post-traumatic stress disorder: from core mechanisms to clinical translation.
Moving beyond the HPA axis, we situate it within a broader neuroendocrine network, reviewing its complex interactions with the hypothalamic-pituitary-thyroid (HPT) axis, the hypothalamic-pituitary-gonadal (HPG) axis, and the sympathetic-adrenal-medullary (SAM) system, as well as with neuropeptides including neuropeptide Y (NPY), orexin, and arginine vasopressin (AVP).
Research status + gaps
What still needs better answers?
- No publishable claim yet for: administration, contraindication, interaction, regulatory, safety
- 146 compiled claim(s) withheld by automated assurance: assurance_score_below_0.58 (117), assurance_score_below_0.72 (24), current_regulatory_source_required (19), extraction_ambiguity (95), high_risk_requires_regulatory_or_two_independent_sources (28), no_direct_support (140), proposal_not_staged (1)
These are the limits of this profile, not an exhaustive list of scientific uncertainties.
References + discovery
Open the records yourself.
- The Effect of Respiratory Muscle Performance on Cognitive Functions in Children with Epilepsy: Monitoring with Glymphatic System Activation and Neuropeptides ↗
clinicaltrials · published 2024-10-15 · retrieved 2026-09-05T09:00:33Z
- IUPHAR interactions for neuropeptide Y ↗
iuphar-interactions · published 2026-08-28 · retrieved 2026-08-28T12:35:21Z
- neuropeptide Y ↗
iuphar-ligand · published 2026-08-28 · retrieved 2026-08-28T12:35:21Z
- The gut-brain axis in avian appetite regulation: Integrating peripheral signals with central neurocircuitry. ↗
pubmed · published 2026-09-01 · retrieved 2026-08-26T20:13:52Z
- Stabilized thioamide peptide agonists of the neuropeptide Y type 2 receptor for targeted cancer imaging. ↗
pubmed · published 2026-08-05 · retrieved 2026-09-05T09:00:33Z
- Plasticity in Thoracic Paravertebral Sympathetic Postganglionic Neurons after High Spinal Cord Transection. ↗
pubmed · published 2026-08-12 · retrieved 2026-09-05T09:00:33Z
- Molecular alterations in chondrolectin-containing somatostatin neurons in schizophrenia differ based on circuit context. ↗
pubmed · published 2026-08-10 · retrieved 2026-09-05T09:00:33Z
- The neuroendocrine network imbalance in post-traumatic stress disorder: from core mechanisms to clinical translation. ↗
pubmed · published 2026-08-13 · retrieved 2026-09-05T09:00:33Z
- The Role of Hippocampal Interneuron Migration in Neurodevelopmental Disorders: A Systematic Review. ↗
pubmed · published 2026-09-01 · retrieved 2026-08-28T12:35:21Z
- Neuropeptide Y regulates myocardial fibrosis via NPY1R/JAK2/STAT3 signaling pathway. ↗
pubmed · published 2026-08-18 · retrieved 2026-09-05T09:00:33Z
- Impact of serotonin transporter deficiency on parvalbumin- and neuropeptide Y-producing neurons of the lateral and basolateral amygdalar nuclei. ↗
pubmed · published 2026-08-19 · retrieved 2026-09-05T09:00:33Z
- A multi-level machine learning pipeline for prediction and prioritization of hybrid insulin peptides in type 1 diabetes. ↗
pubmed · published 2026-01-01 · retrieved 2026-09-05T09:00:33Z
- From Self-Assembly to Survival: Neuropeptide Precursor Biology in Neuroprotection. ↗
pubmed · published 2026-08-05 · retrieved 2026-08-26T20:13:52Z
- Acetylated starch promotes satiety by inhibiting hypothalamic agouti-related peptide and neuropeptide Y neurons. ↗
pubmed · published 2026-08-24 · retrieved 2026-09-05T09:00:33Z
- Disruption of gut bacteria-derived hydrogen sulfide signaling mediates antibacterial-induced acute anorexia. ↗
pubmed · published 2026-08-29 · retrieved 2026-09-05T09:00:33Z
- Exercise-induced neuropeptidergic and neurochemical neuroadaptation in stress regulation and emotional disorders. ↗
pubmed · published 2026-09-02 · retrieved 2026-09-05T09:00:33Z
Publication history and provenance
Version 3 · Automated assessment · 2026-09-05T09:00:33Z
7ae24288a519ad9d904f0739988f2ef209630586d35046eeafea742765c1539e