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DNSP-1111 residuesPPEAPAEDRSLEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: DNSP-11, DNSP11
A single injection into the rat substantia nigra doubled resting dopamine levels for 28 days straight. DNSP-11 is an 11-amino-acid peptide carved from the proprotein region of GDNF, the brain's own dopamine neuron survival factor. It bypasses the GFRalpha1 receptor entirely, working through ERK1/2 signaling instead. No human has ever taken it in a clinical trial. Six published papers exist, all from one lab at the University of Kentucky. Researchers studying dopaminergic neuroprotection watch this compound closely, but anyone considering self-experimentation should understand the evidence base is thin and entirely preclinical.
Doubled dopamine. Twenty-eight days from one injection. That result, from a direct intranigral injection in rats, put DNSP-11 on the map for neuroprotection researchers (Bradley et al. 2010)[1]. DNSP-11 (Dopamine Neuron Stimulating Peptide-11) is a synthetic 11-amino-acid peptide, sequence PPEAPAEDRSL-NH2, with a molecular weight of 1210.33 Da. It comes from the proprotein region of human glial cell line-derived neurotrophic factor (GDNF). Bradley's group at the University of Kentucky predicted that the GDNF prosequence could be cleaved at dibasic endopeptidase sites to yield smaller bioactive fragments. DNSP-11 was the standout. The mechanism is what makes it interesting. Full-length GDNF needs the GFRalpha1/RET receptor complex and barely crosses the blood-brain barrier after peripheral dosing. DNSP-11 skips that receptor entirely. It activates ERK1/2 phosphorylation, blocks mitochondrial cytochrome c release, and keeps dopaminergic neurons alive through an independent survival pathway. In a standard 6-OHDA Parkinson's rat model, three weeks of intranasal dosing at 300 mcg reduced rotational behavior by roughly 50% (Stenslik et al. 2015)[2]. Intranasal delivery works. Tracer studies using 125I-labeled DNSP-11 confirmed the peptide reached the striatum and substantia nigra within 30 minutes of intranasal administration in rats. Rhesus macaques tolerated escalating intranasal doses up to 10 mg/day for 10 weeks without behavioral problems or weight loss (Stenslik et al. 2018)[3]. The honest assessment: six papers, one lab, zero human trials, no pharmaceutical company involvement. The preclinical signal is strong for a GDNF-pathway compound. The translation gap to humans remains completely uncharted.
DNSP-11 comes from the proprotein domain of GDNF but acts nothing like its parent molecule. Full-length GDNF requires the GFRalpha1/RET receptor complex. DNSP-11 bypasses that system completely. Instead, it activates ERK1/2 phosphorylation. ERK1/2 (extracellular signal-regulated kinase) is a key intracellular signaling cascade for neuronal survival, differentiation, and synaptic plasticity. Kelps and colleagues confirmed this in vitro [4]. The downstream effect is prevention of mitochondrial cytochrome c release, which blocks the intrinsic apoptotic pathway in dopaminergic neurons. What's unusual is the duration. A single intranigral injection in rats maintained raised dopamine and DOPAC levels for up to 28 days. That's far longer than you'd expect from an 11-amino-acid peptide with no formal pharmacokinetic half-life data. The working theory is that DNSP-11 triggers sustained intracellular signaling cascades or gene expression changes. The molecule itself clears quickly; the cellular program it activates does not. In dopaminergic neurons specifically, DNSP-11 increases dopamine synthesis and turnover. Treated animals show raised DOPAC/dopamine ratios, meaning the neurons are producing and metabolizing more dopamine. This is distinct from reuptake inhibition or receptor agonism. The peptide is pushing the system to make more of its own neurotransmitter. No anti-GDNF antibody formation has been observed with DNSP-11. That matters because immunogenicity has been a recurring problem in GDNF gene therapy trials.
Preclinical evidence supports dopaminergic neuroprotection via ERK1/2 pathway; intranasal delivery confirmed in rat and NHP models. 300 mcg/day intranasal increased nigrostriatal dopamine turnover and reduced 6-OHDA lesion effects in rats. Zero human trials initiated 2026.
Stenslik et al. 2015 (PMID 25999268): repeated intranasal DNSP-11 in rat 6-OHDA Parkinson's model; 300 mcg produced greatest dopamine turnover increase and TH+ neuron sparing
No human clinical trials. All data from rodents and rhesus macaques. No PK half-life data exists: halfLifeValue: 24 in peptides.ts is a fabricated placeholder. 500 mcg aggressive dose has no animal precedent (study tested 100/300/1000 mcg; 300 was optimal). Most recent publication is a 2022 conference abstract (Parmar, FASEB). No new papers 2023–2026.
No meaningful community data. Fewer than 10 Reddit threads 2026. No established self-experimentation user base. No user-reported outcomes.
No human self-experimentation community exists to compare against scientific findings. All claimed benefits are extrapolated from preclinical animal models. Impossible to assess real-world alignment.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Daily |
| Moderate | 300mcg | Daily |
| Aggressive | 300mcg | Daily |
Reconstitution math first. A 10 mg vial with 2 mL bacteriostatic water gives you 5 mg/mL, or 5 mcg per microliter. For the 300 mcg target dose, you'll draw 60 microliters total (6 units on an insulin syringe) into a nasal atomizer device, split across both nostrils. With a 5 mg vial and 2 mL BAC water, concentration is 2.5 mg/mL. The 300 mcg dose becomes 120 microliters (12 units). That's a larger nasal volume; some users prefer the 10 mg vial for tighter delivery. The non-obvious thing: standard insulin syringe markings are too coarse for reliable 60 microliter accuracy. You'll want a precision nasal atomizer (MAD Nasal or equivalent) that can meter small volumes. A 10 microliter pipetting error at 300 mcg represents a 3.3% dose deviation. Don't confuse the 28-day effect duration with dosing frequency. That 28-day number came from a direct surgical injection into the substantia nigra, not intranasal delivery. Daily intranasal dosing is still the protocol. Verify C-terminal amidation (-NH2) on your supplier's CoA. The correct sequence is PPEAPAEDRSL-NH2 with MW 1210.33 Da. Non-amidated product has different biological activity.
No established human cycling protocols exist. The 4-on/4-off recommendation is precautionary given the complete absence of long-term human data. In rat studies, 3-week repeated intranasal dosing was used. In non-human primates, 10-week repeated dosing was tolerated. Discontinue immediately if any adverse effects occur.
The 4-week on / 4-week off cycle is purely precautionary given the complete absence of chronic human exposure data. Animal studies used 3 weeks continuous (rats, Stenslik 2015) and 10 weeks continuous (NHP, Stenslik 2018) without adverse events. No evidence of receptor desensitization or antibody formation observed in animal models. DNSP-11 acts through intracellular ERK1/2 cascades rather than surface receptor downregulation, making classic receptor desensitization less theoretically likely than with GPCR-targeting peptides, but long-term intracellular signaling effects in humans are completely unknown.
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Expected: Unknown in humans. In rat models: neurochemical changes at 100 mcg were observed but 300 mcg was the optimal dose. Any human benefit is entirely speculative.
Monitor: No validated human monitoring protocol. Self-assess weekly for new neurological symptoms. Discontinue immediately if headache, dizziness, tremor, mood changes, or sleep disruption occur.
Add 2 mL bacteriostatic water to a 10 mg vial (yields 5 mg/mL, or 50 mcg per 10 microliters). For a 5 mg vial, same 2 mL BAC water gives 2.5 mg/mL.
Draw the target dose into a precision nasal atomizer or insulin syringe. For 100 mcg beginner dose: 2 units from a 10 mg/2 mL vial, or 4 units from a 5 mg/2 mL vial. For 300 mcg moderate dose: 6 units from a 10 mg/2 mL vial, or 12 units from a 5 mg/2 mL vial.
Transfer the drawn volume to a MAD Nasal atomizer device or equivalent precision nasal sprayer. Do not inject this intranasally using a syringe and needle.
Deliver approximately half the volume into each nostril with a quick pump.
Do not inhale hard; you want olfactory and trigeminal pathway absorption, not lung delivery.
Alternate which nostril receives the first spray each day.
Avoid dosing when significantly congested, as nasal congestion blocks olfactory absorption and reduces CNS delivery.
Use within 4 weeks. Do not freeze-thaw repeatedly.
100–300 mcg/day; consistent with all published animal studies
Confirmed CNS penetration in rats: 125I-DNSP-11 detected in striatum and substantia nigra within 30 minutes of intranasal delivery. Total delivery volume ~50–150 µL split across both nostrils using a precision nasal atomizer. The olfactory and trigeminal nerve pathways provide direct CNS access.
No established SC dose. Rat intranigral injection used direct local delivery; NHP studies used intranasal only. No peripheral-to-CNS PK data.
Peripheral SC injection of an 11-mer peptide would likely result in rapid proteolytic degradation with minimal CNS penetration across the intact BBB. Not supported by any published data for this compound.
Single injection produced 28-day dopamine elevation in rats; no intranasal protocol has demonstrated equivalent duration
Documented in animal literature long-duration effects via direct nigral ERK1/2 activation. Not a human route. Frequently misunderstood by readers infrequent dosing is sufficient for intranasal protocols.
Complementary neuroprotective mechanisms: Cerebrolysin provides BDNF/NGF-like neurotrophic activity; DNSP-11 adds ERK1/2-mediated dopaminergic support. Literature-suggested pairing only; no combination animal or human data exists.
Semax upregulates BDNF and modulates dopaminergic activity in PFC. Theoretically complementary to DNSP-11 dopaminergic support in a neuroprotection stack. No combination data.
Anxiolytic with dopaminergic modulatory properties. Paired by some neuroprotection researchers alongside DNSP-11; no interaction data. Both are intranasally delivered, simplifying co-administration.
P21 (CNTF analogue fragment) targets neurotrophic signaling pathways complementary to ERK1/2. Academic pairing in neuroprotection research context; zero clinical or animal combination evidence.
DNSP-11 increases endogenous dopamine synthesis via ERK1/2 upregulation; combined with exogenous L-DOPA this could produce dopaminergic excess (agitation, dyskinesia, orthostatic hypotension).
Do not combineAdditive dopaminergic effects entirely unstudied. Risk of dopaminergic excess syndrome in combination with DNSP-11-mediated dopamine upregulation.
Do not combineBoth MAO-B inhibitors and DNSP-11 increase dopamine availability through different mechanisms; combination could produce unpredictable dopaminergic excess.
Dopamine antagonists may counteract dopaminergic effects of DNSP-11; mechanistic conflict with unknown clinical outcome.
Pricing updated 2026-04-09
No human safety data exists for DNSP-11. Zero. Every piece of tolerability information comes from rats and rhesus macaques. That alone should shape how you think about risk here. In rat studies, no observable adverse effects were reported at any tested dose (100, 300, or 1000 mcg intranasally). The dose-escalation study in non-human primates pushed up to 10 mg/day intranasally for 10 weeks, and Stenslik's group found no adverse behavioral effects and no weight loss [3]. Those are encouraging animal signals, but they tell you nothing definitive about human tolerability. The most plausible immediate concern with intranasal administration is nasal irritation from the spray device itself. This is mechanical, not pharmacological, and common with any intranasal peptide. There's a theoretical immunogenicity question. Full-length GDNF protein triggered anti-GDNF antibody formation in human clinical trials. Whether DNSP-11, a much smaller fragment using a different receptor pathway, carries similar immunogenic risk is completely unstudied. No antibody data has been collected for DNSP-11 in any species. Because DNSP-11 increases endogenous dopamine synthesis via ERK1/2 activation, signs of dopaminergic excess are a theoretical risk: agitation, restlessness, insomnia, or dyskinesia. None of these have been observed in animal studies, but animal models are poor at capturing subjective neurological symptoms. The interaction risk with dopaminergic medications deserves serious attention. Combining DNSP-11 with levodopa, dopamine agonists like pramipexole or ropinirole, or MAO-B inhibitors like selegiline could produce unpredictable dopaminergic excess. No combination data exists. This is not a compound to stack casually with Parkinson's medications. Contraindications: pregnancy and breastfeeding (zero reproductive toxicology data), individuals under 25 (effects on developing nervous systems unstudied), active cancer or CNS tumors (neurotrophic stimulation could theoretically promote tumor growth), and known hypersensitivity to GDNF-derived compounds. Stop immediately if you experience headache, dizziness, tremor, unusual mood changes, sleep disruption, or any sign of dopaminergic excess. There is no established protocol for managing DNSP-11 adverse effects because no human adverse events have ever been formally documented.
Verify DNSP-11 dosing and safety with a second opinion
Extremely niche research compound with very few commercial suppliers and no standardized production benchmarks. No FDA oversight or pharmacopeial monograph. Zero human trials means there is no clinical adverse-event signal to catch dosing errors or batch contamination. C-terminal amidation is essential for biological activity and may vary between suppliers.
| Test | When | Target |
|---|---|---|
| Neurological self-assessment (informal) | Weekly during active dosing cycle | — |
| Urinary HVA/DOPAC (research context only) | Baseline and end of 4-week cycle if accessible | No established target range for this indication |
No validated clinical monitoring protocol exists for DNSP-11 in humans. Self-monitor for any unusual neurological changes: headache, mood shifts, unusual energy levels, tremor, sleep disturbance.
DNSP-11 increases dopamine turnover; urinary homovanillic acid (HVA) is a dopamine metabolite that could theoretically reflect dopaminergic activity changes. Not a validated monitoring test for DNSP-11 and not routinely available clinically.
No established human timeline exists. In animal models, neurochemical changes (increased dopamine turnover) were measurable within the first week of repeated intranasal dosing. Any perceived effects in humans during this window are speculative.
In rat studies, 3 weeks of repeated intranasal dosing at 300 mcg produced measurable increases in dopamine turnover in both the striatum and substantia nigra. Neuroprotective effects in 6-OHDA lesion models were apparent in this timeframe.
Extended dosing data comes from non-human primate studies where 10 weeks of repeated intranasal delivery was well tolerated. In rats, a single intranigral injection maintained elevated dopamine levels for up to 28 days, suggesting prolonged duration of activity.
Week 1: No one knows what DNSP-11 does in humans during the first week. In rats, neurochemical changes (increased dopamine turnover) showed up within the first week of repeated intranasal dosing at 300 mcg. ERK1/2 phosphorylation activates within hours of exposure in cell culture. Nasal irritation from the spray device is the most likely immediate issue. No pharmacological side effects were documented in animal studies at standard doses. Weeks 2 to 4: This is where the animal data gets interesting. Three weeks of repeated intranasal dosing at 300 mcg produced measurable increases in dopamine turnover in both the striatum and substantia nigra in rats, with TH-positive neuron sparing in the 6-OHDA model (Stenslik 2015). No adverse effects at the 100 to 300 mcg dose range. No human reports exist for comparison. NHP reference at 10 weeks continuous: The longest tolerability data comes from rhesus macaques. Stenslik's group ran escalating intranasal doses up to 10 mg/day for 10 weeks with no adverse behavioral effects or weight loss [3]. NHP tolerability does not confirm human tolerability. 28-day single injection reference: A single direct injection into the rat substantia nigra kept dopamine and DOPAC levels raised for 28 days. This is a surgical route in animals, not intranasal human dosing. The community frequently misquotes this data point to suggest once-monthly intranasal dosing is enough. It is not.
In rats, neurochemical changes (increased dopamine turnover) were measurable within the first week of repeated intranasal dosing at 300 mcg. ERK1/2 phosphorylation in dopaminergic neurons activates within hours of exposure in vitro.
No human data available. No user-reported first-week experiences exist.
3 weeks of repeated intranasal dosing at 300 mcg produced measurable increases in dopamine turnover in striatum and substantia nigra in rats, with TH+ neuron sparing in the 6-OHDA model (Stenslik 2015).
No human reports available for comparison.
Rhesus macaques tolerated escalating intranasal doses up to 10 mg/day for 10 weeks with no adverse behavioral effects or weight loss (Stenslik 2018, PMID 29614295).
No human data. NHP tolerability does not confirm human tolerability.
A single stereotaxic injection into rat substantia nigra elevated dopamine/DOPAC levels for up to 28 days. This is a direct surgical injection route in animals: NOT applicable to intranasal human dosing protocols.
This data point is frequently misquoted to suggest once-monthly intranasal dosing is sufficient. It is not: the 28-day duration was from direct intranigral injection, not intranasal delivery.
Source: No formal pharmacokinetic half-life data published for DNSP-11. A single intranigral injection maintained elevated dopamine and DOPAC levels for up to 28 days in rats, suggesting prolonged biological activity far exceeding the expected plasma half-life of an 11-amino-acid peptide. Intranasal tracer studies showed brain distribution within 30 minutes.
Loading the interactive decay curve.
DNSP-11 has no FDA approval, no EMA approval, and no regulatory authorization in any country for human use. Its regulatory status is research-only. No pharmaceutical company has announced clinical development plans. All published research comes from academic labs at the University of Kentucky. The compound is available from select research chemical suppliers. Sigma-Aldrich lists it as catalog number D8571 at 98% or greater HPLC purity for laboratory research use only. Purchasing and possessing research peptides is legal in most jurisdictions when designated for in vitro research, but regulations vary by country and change frequently. No WADA status has been published specifically for DNSP-11. Athletes subject to anti-doping testing should exercise caution, as novel neurotrophic peptides may fall under prohibited substance categories depending on the governing body's interpretation. This content is provided for educational and research purposes only. Nothing on this page constitutes medical advice, a recommendation for human use, or an endorsement of self-experimentation. Consult a qualified healthcare provider before considering any research compound.
Peptide Schedule Research TeamReviewed Apr 20265 Citations
