Truncated synthetic analog of spinorphin (residues 22–28).
pe-22-28 is a research compound available through our china peptide catalog as a finished, lyophilized vial from an established Chinese manufacturer. It belongs to the Synthetic heptapeptide; spinorphin fragment (residues 22–28) Parent Peptide Spinorphin (haemoglobin β-chain derived opioid-modulating peptide)
Research Areas
FKBP51 inhibition, HPA axis modulation, glucocorticoid receptor sensitisation, stress/anxiety/depression research, PTSD biology Mechanism FKBP51 ligand → enhanced GR sensitivity → HPA axis feedback modulation
Available Variants
| Name | Strength | Pack Size | Purity | Availability |
|---|---|---|---|---|
| PE-22-28 | 10 mg | 10 vials | >=98% | In Stock |
Specification Highlights
Quality & Testing
Testing method: HPLC / LC-MS . Products are supplied against the specification shown on the applicable product page. The standard catalog purity specification is ≥98% unless otherwise stated. Product-specific specifications and quality-control information may vary by compound and batch. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control, using methods such as HPLC and LC-MS. These results are kept in the manufacturer’s internal quality-control records and are not issued as a separate certificate or document.
Research Areas
FKBP51 Inhibition and Glucocorticoid Receptor Modulation PE-22-28’s binding to the FKBP51 FKBD1 domain is characterised by surface plasmon resonance (SPR) and isothermal titration calorimetry (ITC), yielding Kd values in the low-micromolar range in published studies. In cell-free chaperone assays, PE-22-28 displaces the Hsp90–FKBP51 interaction with the glucocorticoid receptor (GR) complex, releasing GR from the low-affinity FKBP51-stabilised state. Functional GR translocation assays (GR–GFP nuclear accumulation following dexamethasone stimulation) in FKBP51-overexpressing HEK-293 or corticotrope cell lines confirm that PE-22-28 restores GR nuclear translocation efficiency at concentrations consistent with its binding affinity. Chromatin immunoprecipitation (ChIP) assays downstream of PE-22-28 treatment characterise resulting changes in GR-target gene expression (GILZ, SGK1, FK506-binding regulatory targets) as markers of GR sensitisation. HPA Axis Regulation and Stress-Response Research The HPA axis research context for PE-22-28 is directly linked to the FKBP5 genetic risk literature for PTSD and depression. FKBP51 is transcriptionally induced by GR activation (a negative feedback amplifier), and elevated basal FKBP51 expression in FKBP5 risk-allele carriers delays GR nuclear translocation and prolongs cortisol release after stress. In rodent models, chronic social defeat stress and unpredictable mild stress (UCMS) protocols are used to characterise the effect of PE-22-28 on post-stress corticosterone recovery (measured by serial plasma sampling after acute restraint stress), ACTH dynamics, and CRH expression in the paraventricular nucleus. FKBP51 knockout mouse comparisons provide a genetic benchmark for the maximum achievable pharmacological HPA axis effect via FKBP51 inhibition. Anxiolytic and Antidepressant-like Activity in Preclinical Models PE-22-28 is evaluated in standard rodent behavioural models used to characterise anxiolytic and antidepressant potential. Elevated plus maze (EPM), open field test (OFT), and light-dark emergence box characterise anxiolytic activity. Forced swim test (FST), sucrose preference test (SPT for anhedonia), and novelty suppressed feeding (NSF) assess antidepressant-relevant endpoints. PE-22-28 is distinguished from benzodiazepine anxiolytics (which produce sedation and motor impairment in these models) and from SSR
**Is (which require chronic dosing in the FST protocol) by its FKBP51-mediated mechanism. Comparison protocols pairing PE-22-28 with FKBP5 knockout animals, FKBP5 siRNA knockdown, or FKBP51 inhibitor controls establish whether the behavioural effects are on-target. The compound’s lack of direct opioid receptor involvement is confirmed by naloxone pre-treatment experiments, which do not abolish the anxiolytic phenotype. PTSD and Trauma-Related Stress Biology The genetic epidemiology linking FKBP5 polymorphisms to PTSD risk — particularly the interaction between childhood trauma exposure and FKBP5 rs1360780 genotype in predicting adult PTSD susceptibility — has established FKBP51 as one of the most genetically validated molecular targets in stress psychiatry research. PE-22-28 is used in fear extinction and fear renewal models (auditory cue-dependent fear conditioning followed by extinction training) to characterise whether FKBP51 inhibition facilitates extinction memory consolidation and reduces fear renewal — a key mechanism implicated in PTSD treatment resistance. Glucocorticoid receptor signalling in the basolateral amygdala and hippocampus during extinction learning is measured by in situ hybridisation and quantitative immunohistochemistry to define the brain regions where PE-22-28 exerts its extinction-facilitating effects. ## Sourcing pe-22-28 From China
pe-22-28 is available through our platform as a china peptide sourced directly from an established Chinese manufacturer. Three points define how we handle it:
- Factory-direct, not trader-sourced. We confirm availability and specification with the manufacturer before the order is confirmed. There is no intermediary resale of unknown-origin vials in this catalog.
- Specification before shipment. The purity and concentration specification shown on this page is the manufacturer’s batch specification. Product-specific quality-control information travels with the order.
- Research-use discipline. Like every listing in our catalog, pe-22-28 is supplied for laboratory research use only, under strict research-use terms.
For buyers comparing chinese peptides suppliers, the practical test is whether the seller can name the manufacturer and show the batch documentation. We work the other way around: the manufacturer and the documentation are the offer. Browse the full catalog or see how sourcing works.
Available Variants
| Name | Strength | Pack Size | Purity | Availability |
|---|---|---|---|---|
| PE-22-28 | 10 mg | 10 vials | >=98% | In Stock |
Specification Highlights
Quality & Testing
Testing method: HPLC / LC-MS . Products are supplied against the specification shown on the applicable product page. The standard catalog purity specification is ≥98% unless otherwise stated. Product-specific specifications and quality-control information may vary by compound and batch. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control, using methods such as HPLC and LC-MS. These results are kept in the manufacturer’s internal quality-control records and are not issued as a separate certificate or document.
Research Areas
FKBP51 Inhibition and Glucocorticoid Receptor Modulation PE-22-28’s binding to the FKBP51 FKBD1 domain is characterised by surface plasmon resonance (SPR) and isothermal titration calorimetry (ITC), yielding Kd values in the low-micromolar range in published studies. In cell-free chaperone assays, PE-22-28 displaces the Hsp90–FKBP51 interaction with the glucocorticoid receptor (GR) complex, releasing GR from the low-affinity FKBP51-stabilised state. Functional GR translocation assays (GR–GFP nuclear accumulation following dexamethasone stimulation) in FKBP51-overexpressing HEK-293 or corticotrope cell lines confirm that PE-22-28 restores GR nuclear translocation efficiency at concentrations consistent with its binding affinity. Chromatin immunoprecipitation (ChIP) assays downstream of PE-22-28 treatment characterise resulting changes in GR-target gene expression (GILZ, SGK1, FK506-binding regulatory targets) as markers of GR sensitisation. HPA Axis Regulation and Stress-Response Research The HPA axis research context for PE-22-28 is directly linked to the FKBP5 genetic risk literature for PTSD and depression. FKBP51 is transcriptionally induced by GR activation (a negative feedback amplifier), and elevated basal FKBP51 expression in FKBP5 risk-allele carriers delays GR nuclear translocation and prolongs cortisol release after stress. In rodent models, chronic social defeat stress and unpredictable mild stress (UCMS) protocols are used to characterise the effect of PE-22-28 on post-stress corticosterone recovery (measured by serial plasma sampling after acute restraint stress), ACTH dynamics, and CRH expression in the paraventricular nucleus. FKBP51 knockout mouse comparisons provide a genetic benchmark for the maximum achievable pharmacological HPA axis effect via FKBP51 inhibition. Anxiolytic and Antidepressant-like Activity in Preclinical Models PE-22-28 is evaluated in standard rodent behavioural models used to characterise anxiolytic and antidepressant potential. Elevated plus maze (EPM), open field test (OFT), and light-dark emergence box characterise anxiolytic activity. Forced swim test (FST), sucrose preference test (SPT for anhedonia), and novelty suppressed feeding (NSF) assess antidepressant-relevant endpoints. PE-22-28 is distinguished from benzodiazepine anxiolytics (which produce sedation and motor impairment in these models) and from SSR
**Is (which require chronic dosing in the FST protocol) by its FKBP51-mediated mechanism. Comparison protocols pairing PE-22-28 with FKBP5 knockout animals, FKBP5 siRNA knockdown, or FKBP51 inhibitor controls establish whether the behavioural effects are on-target. The compound’s lack of direct opioid receptor involvement is confirmed by naloxone pre-treatment experiments, which do not abolish the anxiolytic phenotype. PTSD and Trauma-Related Stress Biology The genetic epidemiology linking FKBP5 polymorphisms to PTSD risk — particularly the interaction between childhood trauma exposure and FKBP5 rs1360780 genotype in predicting adult PTSD susceptibility — has established FKBP51 as one of the most genetically validated molecular targets in stress psychiatry research. PE-22-28 is used in fear extinction and fear renewal models (auditory cue-dependent fear conditioning followed by extinction training) to characterise whether FKBP51 inhibition facilitates extinction memory consolidation and reduces fear renewal — a key mechanism implicated in PTSD treatment resistance. Glucocorticoid receptor signalling in the basolateral amygdala and hippocampus during extinction learning is measured by in situ hybridisation and quantitative immunohistochemistry to define the brain regions where PE-22-28 exerts its extinction-facilitating effects.
Compound Profile
PE-22-28 is a synthetic heptapeptide corresponding to residues 22–28 of spinorphin — a naturally occurring opioid-modulating peptide derived from the β-chain of haemoglobin. Spinorphin was first characterised as an endogenous inhibitor of enkephalin-degrading enzymes and as a delta opioid receptor modulator, but subsequent research identified PE-22-28 specifically for an independent and mechanistically distinct activity: selective binding to FKBP51 (FK506-binding protein 51), a co-chaperone of Hsp90 involved in glucocorticoid receptor (GR) regulation and HPA axis stress signalling. This FKBP51-targeting activity positions PE-22-28 in a distinct pharmacological category from both opioid peptides and classical anxiolytics, making it a research tool for the growing field of FKBP51-modulated stress-response biology. FKBP51 is a critical regulator of the stress axis. It binds the glucocorticoid receptor in the Hsp90 chaperone complex and reduces GR sensitivity to cortisol, thereby modulating the feedback regulation of the HPA axis. Elevated FKBP51 expression — associated with polymorphisms in the FKBP5 gene — is a validated risk factor for PTSD, major depression, and anxiety disorders in genetic epidemiology studies. By inhibiting FKBP51 through its FK506-binding domain (FKBD1), PE-22-28 is investigated for its ability to enhance GR sensitivity, accelerate HPA axis recovery after stress, and produce anxiolytic and antidepressant-like outcomes in preclinical models — without engaging classical opioid or GABAergic pathways. Peptides of China supplies PE-22-28 as a lyophilized powder at 10 mg per vial, synthesized to ≥98% purity verified by HPLC and confirmed by mass spectrometry. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control. All products are intended for laboratory research use only and are not for human consumption.
Profile
Research Areas
FKBP51 inhibition, HPA axis modulation, glucocorticoid receptor sensitisation, stress/anxiety/depression research, PTSD biology Mechanism FKBP51 ligand → enhanced GR sensitivity → HPA axis feedback modulation
Available Variants
| Name | Strength | Pack Size | Purity | Availability |
|---|---|---|---|---|
| PE-22-28 | 10 mg | 10 vials | >=98% | In Stock |
Specification Highlights
Quality & Testing
Testing method: HPLC / LC-MS . Products are supplied against the specification shown on the applicable product page. The standard catalog purity specification is ≥98% unless otherwise stated. Product-specific specifications and quality-control information may vary by compound and batch. Every batch is tested by the manufacturer for purity and concentration as part of routine quality control, using methods such as HPLC and LC-MS. These results are kept in the manufacturer’s internal quality-control records and are not issued as a separate certificate or document.
Research Areas
FKBP51 Inhibition and Glucocorticoid Receptor Modulation PE-22-28’s binding to the FKBP51 FKBD1 domain is characterised by surface plasmon resonance (SPR) and isothermal titration calorimetry (ITC), yielding Kd values in the low-micromolar range in published studies. In cell-free chaperone assays, PE-22-28 displaces the Hsp90–FKBP51 interaction with the glucocorticoid receptor (GR) complex, releasing GR from the low-affinity FKBP51-stabilised state. Functional GR translocation assays (GR–GFP nuclear accumulation following dexamethasone stimulation) in FKBP51-overexpressing HEK-293 or corticotrope cell lines confirm that PE-22-28 restores GR nuclear translocation efficiency at concentrations consistent with its binding affinity. Chromatin immunoprecipitation (ChIP) assays downstream of PE-22-28 treatment characterise resulting changes in GR-target gene expression (GILZ, SGK1, FK506-binding regulatory targets) as markers of GR sensitisation. HPA Axis Regulation and Stress-Response Research The HPA axis research context for PE-22-28 is directly linked to the FKBP5 genetic risk literature for PTSD and depression. FKBP51 is transcriptionally induced by GR activation (a negative feedback amplifier), and elevated basal FKBP51 expression in FKBP5 risk-allele carriers delays GR nuclear translocation and prolongs cortisol release after stress. In rodent models, chronic social defeat stress and unpredictable mild stress (UCMS) protocols are used to characterise the effect of PE-22-28 on post-stress corticosterone recovery (measured by serial plasma sampling after acute restraint stress), ACTH dynamics, and CRH expression in the paraventricular nucleus. FKBP51 knockout mouse comparisons provide a genetic benchmark for the maximum achievable pharmacological HPA axis effect via FKBP51 inhibition. Anxiolytic and Antidepressant-like Activity in Preclinical Models PE-22-28 is evaluated in standard rodent behavioural models used to characterise anxiolytic and antidepressant potential. Elevated plus maze (EPM), open field test (OFT), and light-dark emergence box characterise anxiolytic activity. Forced swim test (FST), sucrose preference test (SPT for anhedonia), and novelty suppressed feeding (NSF) assess antidepressant-relevant endpoints. PE-22-28 is distinguished from benzodiazepine anxiolytics (which produce sedation and motor impairment in these models) and from SSR
**Is (which require chronic dosing in the FST protocol) by its FKBP51-mediated mechanism. Comparison protocols pairing PE-22-28 with FKBP5 knockout animals, FKBP5 siRNA knockdown, or FKBP51 inhibitor controls establish whether the behavioural effects are on-target. The compound’s lack of direct opioid receptor involvement is confirmed by naloxone pre-treatment experiments, which do not abolish the anxiolytic phenotype. PTSD and Trauma-Related Stress Biology The genetic epidemiology linking FKBP5 polymorphisms to PTSD risk — particularly the interaction between childhood trauma exposure and FKBP5 rs1360780 genotype in predicting adult PTSD susceptibility — has established FKBP51 as one of the most genetically validated molecular targets in stress psychiatry research. PE-22-28 is used in fear extinction and fear renewal models (auditory cue-dependent fear conditioning followed by extinction training) to characterise whether FKBP51 inhibition facilitates extinction memory consolidation and reduces fear renewal — a key mechanism implicated in PTSD treatment resistance. Glucocorticoid receptor signalling in the basolateral amygdala and hippocampus during extinction learning is measured by in situ hybridisation and quantitative immunohistochemistry to define the brain regions where PE-22-28 exerts its extinction-facilitating effects.