DNSP-11

Dosing from the Literature

Published for Parkinson’s disease: animal doses only — single 30 µg and 100 µg injections into the substantia nigra of rats (Bradley et al., 2010), 300 µg a day into the nose of rats (Stenslik et al., 2015), and up to 10 mg a day into the nose of rhesus macaques (Stenslik et al., 2018). Not published: any human dose, and no DNSP-11 trial is registered (ClinicalTrials.gov, searched October 4, 2026).

The table records each dose as the study gave it, with the species. No label and no trial document exists, because no person has received DNSP-11.

What It Is

DNSP-11 is a synthetic peptide of 11 amino acids — proline-proline-glutamate-alanine-proline-alanine-glutamate-aspartate-arginine-serine-leucine (PPEAPAEDRSL), with an amide at its C-terminal end — made to order and purified by reverse-phase HPLC — to over 98% in the studies that state a purity (Bradley et al., 2010; Kelps et al., 2011; Stenslik et al., 2015). Its mass was calculated at 1,180 Da and measured at 1,180.3 Da by mass spectrometry (Kelps et al., 2011). The sequence is not invented: it sits at positions 28–38 of the 211-amino-acid human pre-proGDNF protein, the precursor of glial cell line-derived neurotrophic factor (UniProt P39905), immediately after a pair of basic residues. Its discoverers read the precursor for internal dibasic cleavage sites and predicted that enzymes would cut out an 11-amino-acid amidated peptide, which they named dopamine neuron stimulating peptide-11 (Bradley et al., 2010). Two sibling peptides were predicted the same way: DNSP-5 (FPLPA-amide, 542 Da) from the prodomain and DNSP-17 (ERNRQAAAANPENSRGK-amide, 1,868 Da) from the start of the mature protein (Kelps et al., 2011). Up to 2011 none of the three had been isolated from tissue, and the authors said so: the peptides "have not been isolated endogenously to date" (Kelps et al., 2011).

The reason anyone looked is GDNF’s own record. GDNF was purified in 1993 as a factor that kept midbrain dopamine neurons alive (Lin et al., 1993), and it protected and restored dopamine neurons in rodents and monkeys well enough to reach the clinic. In people the results split. Five patients given GDNF directly into the putamen in a Phase 1 safety trial improved (Gill et al., 2003), and 10 patients in a University of Kentucky open-label study improved by 33–34% on the total Unified Parkinson’s Disease Rating Scale at 24 weeks (Slevin et al., 2005). Then a randomized trial in 34 patients found a 10.0% improvement in the off-state motor score against 4.5% on placebo (p = 0.53) (Lang et al., 2006), and a randomized trial found 17.3% against 11.8% (p = 0.41) in its 35-patient primary analysis, despite a 25–100% rise in 18F-DOPA uptake in the putamen (Whone et al., 2019). The explanation the field reached for is delivery: GDNF is large and binds heparin tightly, so it spreads poorly from an infusion catheter (Bradley et al., 2010; Kelps et al., 2011). A small, stable peptide that did some of GDNF’s work would not need the catheter.

DNSP-11 came out of the group that ran the Kentucky GDNF study: Don Gash, Greg Gerhardt and Luke Bradley at the University of Kentucky, with John Glass (Bradley et al., 2010; Slevin et al., 2005). The same three are named on two granted US patents assigned to the University of Kentucky Research Foundation, both claiming priority to an application of October 27, 2006: US 9,402,875 B2, granted August 2, 2016, and US 9,586,992 B2, granted March 7, 2017, whose claims cover giving the peptide for Parkinson’s disease, Alzheimer’s disease and ALS, and nasally after traumatic brain injury. Independently, a Helsinki group had predicted the rat counterpart of the same sequence, named it brain excitatory peptide (BEP), and reported that it increased synaptic excitation in rat hippocampal CA1 neurons (Immonen et al., 2008).

The whole literature is small. PubMed returns 8 records for "DNSP-11" (October 4, 2026): six are studies of the peptide itself (Bradley et al., 2010; Kelps et al., 2011; Fuqua et al., 2014; Stenslik et al., 2015; Stenslik et al., 2018; Sonne et al., 2019), one is a test-tube study of amyloid aggregation that used it (Liu et al., 2023), and one is a Russian-language review of GDNF isoforms (Parshina et al., 2025). Europe PMC returns 14 records for the exact phrase: the same six primary papers, five reviews, and three research papers on other peptides and on GDNF itself that mention it in passing (searched October 4, 2026). The peptide still appears in reviews as a candidate: a 2024 review of intranasal treatments for Parkinson’s disease lists it among the synthetic peptides tested in animals (Wen & Ren, 2024), and a 2026 paper on GDNF-receptor peptides names it as one of the few reported GDNF peptide mimetics drawn from the native sequence (Atkinson et al., 2026). No company has taken it up, and no trial has been registered (ClinicalTrials.gov, searched October 4, 2026).

Mechanism of Action

Everything below comes from cell cultures, cell-free assays, rat tissue and live rats and monkeys, and most of it from one group’s laboratories (Bradley et al., 2010; Kelps et al., 2011; Fuqua et al., 2014; Stenslik et al., 2018). Nothing has been measured in a person (PubMed and ClinicalTrials.gov, searched October 4, 2026), and the receptor it works through, if any, is unidentified: reviewers outside the group note that it signals through something other than the GDNF receptor complex (Sidorova & Saarma, 2020).

• Not the GDNF receptor (GFRα1) — Two tests argue against the obvious mechanism. A pull-down assay with biotinylated DNSP-11 and purified GFRα1 showed binding for GDNF and none for the peptide, and a direct ELISA with GFRα1-Fc across a 0–2 µg/mL range showed binding only with GDNF (Bradley et al., 2010). Reviewers outside the group accept the point: DNSP-11 "signals via a different receptor complex than GFRα1/RET" (Sidorova & Saarma, 2020).
• Metabolic proteins, including GAPDH — Biotinylated DNSP-11 incubated with cytosol from the substantia nigra of Fischer 344 rats pulled down 16 proteins identified by mass spectrometry; 11 of them are metabolic enzymes, among them glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and none belongs to the GDNF/GFRα1/RET pathway (Bradley et al., 2010). The group offers this as a hypothesis about mitochondrial and metabolic action, not a demonstrated mechanism (Bradley et al., 2010).
• Mitochondria and cytochrome c — In dopaminergic B65 cells deprived of serum, DNSP-11 at 1 ng/mL reduced the cell death caused by staurosporine (1 µM) and by gramicidin (1 µM), a mitochondrial depolarizing agent, at 20 hours, where GDNF gave no protection (Bradley et al., 2010). In a separate experiment, 10 ng/mL DNSP-11 over six hours kept cytochrome c inside the mitochondria of the same cells exposed to staurosporine (1 µM), where GDNF at 1 ng/mL did not (Bradley et al., 2010).
• Caspase-3, in non-neuronal cells too — In HEK-293 kidney cells, staurosporine (1 µM, 12 hours) raised caspase-3 activity by about 80% and 3-nitropropionate (8 mM) by about 100%; DNSP-11 at 10–100 nM brought caspase-3 back to control values against both, while below 10 nM it did nothing, and the sibling peptides DNSP-5 and DNSP-17 gave no significant protection (Kelps et al., 2011). 3-Nitropropionate blocks succinate dehydrogenase, which the authors read as evidence that the protection runs through mitochondria (Kelps et al., 2011).
• ERK1/2 phosphorylation — In the MN9D dopaminergic cell line, 20 minutes of DNSP-11 at 100 nM raised ERK1/2 phosphorylation by more than 300% over control, and 1 µM by more than 400%, comparable to 1.5 nM GDNF (about 50 ng/mL) (Fuqua et al., 2014). The authors call the potency difference between the two further evidence of a different mechanism (Fuqua et al., 2014).
• No heparin binding — On a heparin affinity column, GDNF eluted at about 0.8 M NaCl and DNSP-17 matched it, while DNSP-11 and DNSP-5 passed straight through with no affinity (Kelps et al., 2011). That is the practical argument for the peptide: heparin binding is what holds GDNF near the catheter tip (Kelps et al., 2011).
• Where the sequence is found in a rat brain — A custom antibody to DNSP-11 stained the substantia nigra pars compacta, ventral tegmental area, dentate gyrus and dorsal raphe of adult Fischer 344 rats, with the strongest signal in the locus ceruleus, where GDNF is not expressed; at postnatal day 10 the DNSP-11 and GDNF signals overlapped extensively but not exclusively (Sonne et al., 2019). A polyclonal antibody raised against the sequence does not distinguish the free peptide from the proGDNF form of it (Bradley et al., 2010), and the mapping study says the specificity of its own antibody is not known (Sonne et al., 2019). Two other proteins carry similar sequences — neuropeptide Y shares five consecutive residues, and the TRK-fused gene product carries PPSAPTEDRSG at its residues 194–206 — and the study’s authors argue that neither of them reproduces the pattern they stained, and that uncut preproGDNF does not explain it either, while allowing that the signal may come from peptides other than DNSP-11 (Sonne et al., 2019).
• The rat counterpart raised synaptic excitation — BEP, the rat version of the sequence (LLEAPAEDHSL-amide), produced a substantial increase in synaptic excitability in rat CA1 pyramidal neurons; the effect was sensitive to N-ethylmaleimide, which the authors read as suggesting a G-protein-coupled receptor (Immonen et al., 2008; sequence as given in Fuqua et al., 2014).

What the Research Shows

The results below are in cell cultures, rats and monkeys (Bradley et al., 2010; Stenslik et al., 2015; Stenslik et al., 2018). There is no human section to compare them with (PubMed and ClinicalTrials.gov, searched October 4, 2026).

• Rat embryo dopamine neurons — In cultures from the ventral mesencephalon of embryonic day 14 Sprague Dawley rats, DNSP-11 across 0.03–10 ng/mL raised the number of surviving tyrosine-hydroxylase-positive neurons; at 0.1 ng/mL the count reached 161% of control (p < 0.05), combined neurite length went from 222 to 306 µm and branches per neuron from 3.1 to 4.4 (p < 0.01 each), while cell-body size did not change, unlike with GDNF (Bradley et al., 2010). The paper’s text describes the survival effect as a 75% increase over control, more than its own table shows at that dose (Bradley et al., 2010).
• Protection against a dopamine neurotoxin in cells — In MN9D dopaminergic cells, one hour of 1 ng/mL DNSP-11 before 15 minutes of 100 µM 6-hydroxydopamine (6-OHDA) reduced both the share of TUNEL-positive cells at 24 hours and caspase-3 activity at 3 hours, as GDNF did (Bradley et al., 2010).
• Normal rats, one injection into the substantia nigra — Twenty-eight days after 30 µg of DNSP-11 went into the right substantia nigra of normal male Fischer 344 rats, microdialysis in the striatum on the same side found resting dopamine at 45.8 ± 7.7 nM against 26.0 ± 2.7 nM on vehicle (p = 0.0314), DOPAC at 6,544 ± 836 against 3,355 ± 338 nM (p = 0.0025) and HVA at 4,516 ± 502 against 2,419 ± 251 nM (p = 0.0012) (Bradley et al., 2010). The paper describes these as rises "by over 100%"; the figures themselves are 76%, 95% and 87% (Bradley et al., 2010).
• Rats with a severe lesion — In Fischer 344 rats given 6-OHDA at two sites along the medial forebrain bundle, which removed over 99% of striatal and over 97% of nigral dopamine, a single 100 µg injection into the substantia nigra cut apomorphine-induced turning by about 50%, significant one week after treatment and holding for the four weeks measured (repeated-measures ANOVA p = 0.0005); at five weeks, nigral dopamine was 74% higher (34.7 ± 6.4 against 59.1 ± 7.3 ng/g, p = 0.0265) and DOPAC 132% higher (7.10 ± 1.40 against 16.48 ± 4.01 ng/g, p = 0.0364), with no change in the lesioned striatum (Bradley et al., 2010).
• The follow-up that found less — Four weeks after 30 µg into the substantia nigra of normal rats, microdialysis found no difference from vehicle in either potassium-evoked or amphetamine-evoked dopamine release, and spontaneous movement — distance travelled and speed — did not change over three weeks (p = 0.10 and p = 0.11) (Fuqua et al., 2014). A more local method, high-speed chronoamperometry, did find more potassium-evoked release two weeks after treatment: 44% above vehicle in the dorsal striatum (p < 0.01) and 52% above a scrambled control peptide in the intermediate striatum (p < 0.05), with nothing at one or four weeks (Fuqua et al., 2014). The same study showed the sequence matters: an 11-mer of the same amino acids in random order behaved like vehicle (Fuqua et al., 2014).
• Into the nose, in rats — Given intranasally five days a week for three weeks to normal rats, 300 µg a day was the lowest dose that raised dopamine turnover in both the striatum (25%) and the substantia nigra (34%), p < 0.05 each, while 1,000 µg a day raised it in the substantia nigra only (Stenslik et al., 2015). In rats lesioned with 6-OHDA at three striatal sites, 300 µg a day — seven days before the lesion and five weeks after it — left d-amphetamine-induced turning 55% lower at two weeks (p < 0.05) and 35% lower at four weeks (not significant), striatal dopamine turnover 39% lower than vehicle (p < 0.01; the paper’s discussion gives 35%), and more surviving tyrosine-hydroxylase-positive neurons in the middle of the substantia nigra pars compacta (29 ± 5 against 13 ± 2, p < 0.05), with no difference rostrally, a non-significant 44% difference caudally and no change in fibre density (Stenslik et al., 2015). A radioiodinated, R9K-modified version of the peptide — the sequence was changed at position 9 so that it could be iodinated — reached cerebrospinal fluid and the striatum and substantia nigra within 30 minutes of a single nasal dose (Stenslik et al., 2015).
• Into the nose, in monkeys — Six female rhesus macaques, 10–18 years old, each given MPTP into one carotid artery in an earlier study, received either DNSP-11 or vehicle by atomizer on four consecutive days a week for 10 weeks, the dose rising from 0.3 to 10 mg a day; three animals got the peptide (Stenslik et al., 2018). On the unlesioned side, DOPAC fell by 59% in the putamen (p = 0.0317), 54% in the caudate (p = 0.0078) and 45% in the nucleus accumbens (p = 0.0017), and HVA by 25%, 24% and 21% in the putamen, caudate and globus pallidus (p = 0.0097, 0.0363, 0.0061), with dopamine itself unchanged; the authors read the fall as a normalization of the compensatory turnover that MPTP produces (Stenslik et al., 2018). On the lesioned side the animals’ lesions were too variable and too few for statistics, and the comparison was left qualitative: two DNSP-11 animals had turnover ratios 2.6–3.8 times those of two comparable vehicle animals, while one vehicle animal was depleted by more than 99% and one DNSP-11 animal had higher dopamine than the rest (Stenslik et al., 2018). In the one animal given the radioiodinated R9K version, signal appeared in the olfactory bulbs and trigeminal nerves and diffusely through the brain by 60 minutes, with twice as much in the pituitary gland as in the olfactory bulbs, and in blood, urine and thyroid (Stenslik et al., 2018).
• In a test tube, against amyloid — A group at the National Institute on Aging, outside the Kentucky team, added DNSP-11 to Thioflavin T aggregation assays: it held islet amyloid polypeptide aggregation to 24.1% of control over the 90–160 minute window (p = 0.003) and amyloid-β 42 aggregation to 61.9% of control over 30–120 minutes (p < 0.0001) (Liu et al., 2023). This is a cell-free assay, with no animal or human follow-up.
• The sibling peptide — DNSP-5, the 5-amino-acid peptide from the same prodomain, increased differentiation markers in embryonic rat dopamine neuron cultures at 0.03–10 ng/mL (p < 0.001) and, as a single 30 µg injection into the rat substantia nigra, raised extracellular striatal dopamine by about 66% at 28 days without changing its metabolites (Littrell et al., 2013). It gave no protection in the HEK-293 caspase-3 assays where DNSP-11 did (Kelps et al., 2011).

Human Data

There is none. No published study has given DNSP-11 to a person, and ClinicalTrials.gov holds no record of a DNSP-11 trial: the registry returns zero records for "DNSP-11" and two unrelated records for the phrase "dopamine neuron stimulating peptide" (searched October 4, 2026). PubMed and Europe PMC return no human study of the peptide (searched October 4, 2026). What follows is the human record of its parent protein, which is a different molecule.

• Nothing of its own — Six published studies of DNSP-11 exist and all are in cells, rat tissue, rats or monkeys (Bradley et al., 2010; Kelps et al., 2011; Fuqua et al., 2014; Stenslik et al., 2015; Stenslik et al., 2018; Sonne et al., 2019). No Phase 1, no healthy-volunteer study and no case report turned up.
• The parent protein, open-label — GDNF infused into the putamen of five patients in a Phase 1 safety trial left their off-medication motor scores 39% better at one year, with a 61% better activities-of-daily-living sub-score and no serious clinical side effects (Gill et al., 2003), and 10 patients in a University of Kentucky study whose total Unified Parkinson’s Disease Rating Scale scores improved 33% off and 34% on at 24 weeks, on 3, 10 and 30 µg a day in eight-week steps (Slevin et al., 2005). Two patients in the latter had transient Lhermitte symptoms (Slevin et al., 2005).
• The parent protein, randomized — A randomized trial gave 34 patients 15 µg per putamen a day or placebo: off-state motor scores improved 10.0% against 4.5%, a difference that was not significant (95% CI −23.0 to 12.0, p = 0.53), despite higher 18F-dopa uptake (Lang et al., 2006). A later randomized trial randomized 41 patients to 120 µg per putamen every four weeks for 40 weeks by convection-enhanced delivery; in its primary analysis, which the protocol limited to 35 of them, off-state motor scores improved 17.3 ± 17.6% against 11.8 ± 15.8% (p = 0.41), and across all 41 a post-hoc count found nine patients on GDNF (43% of that group) with a 10-point or larger improvement against none on placebo (p = 0.0008) (Whone et al., 2019).
• Why that matters here — The peptide exists because the protein’s delivery failed, and the peptide’s own case rests on rat and monkey neurochemistry (Bradley et al., 2010; Stenslik et al., 2015). The GDNF record does not transfer: DNSP-11 showed no binding to GDNF’s receptor and pulled down a different set of proteins (Bradley et al., 2010).
• The evidence meter — The DNSP-11 card reads "Animal only". It counts published human data on DNSP-11 itself, and there is none: not a pilot, not a case series, not a registered trial (ClinicalTrials.gov, PubMed and Europe PMC, searched October 4, 2026).

Reconstitution & Storage

There is nothing to reconstitute for human use: no person has received DNSP-11, and no label or trial document exists (ClinicalTrials.gov, searched October 4, 2026). What is on record is how laboratories handled it.

• What the studies dissolved it in — For injection into the rat brain, DNSP-11 was dissolved at 6 µg/µL (and 20 µg/µL for the lesioned rats) in sterile citrate buffer, 10 mM citrate with 150 mM sodium chloride at pH 5, which also served as the vehicle control (Bradley et al., 2010; Fuqua et al., 2014). For the nasal studies in rats and monkeys it was dissolved in 0.9% sterile saline (Stenslik et al., 2015; Stenslik et al., 2018).
• Stability, as measured — In citrate buffer the peptide was stable at −80 °C and at 37 °C for 31 days: 97.6% of it remained after 30 days at 37 °C, and mass spectrometry at 31 days gave 1,180.3 Da against 1,180 calculated, with no deamidation; a separate test found no degradation after one week at 4 °C (Kelps et al., 2011).
• How long it lasts in a body — Immunostaining for the peptide in the rat substantia nigra faded by three hours after an injection and was undetectable at 24 hours, while the neurochemical changes lasted weeks (Bradley et al., 2010; Fuqua et al., 2014). Its half-life in rat plasma is given as under 12 minutes, reported as unpublished data in the nasal study and repeated in a later review (Stenslik et al., 2015; Sidorova & Saarma, 2020).
• The reagent that is sold — A chemical catalogue lists 1 mg of DNSP-11 trifluoroacetate salt, at least 98% by HPLC, as a white to off-white powder stored at −20 °C, and marks the item discontinued (catalogue listing read October 4, 2026; see Legal Status). No study has tested a product bought from a catalogue, and no independent analysis of one has been published.

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Side Effects & Risks

• In monkeys — Over 10 weeks of nasal dosing rising to 10 mg a day, the three treated macaques showed no nosebleeds, no gastrointestinal irritation, no seizures or dyskinesia and no other behavioural effect on daily cage-side observation, and body weight changed by 5% or less in both groups (Stenslik et al., 2018).
• In rats — The reports describe no adverse effects from single injections into the substantia nigra at 30 and 100 µg (Bradley et al., 2010) or from three weeks of nasal dosing at 100–1,000 µg a day (Stenslik et al., 2015).
• The rat deaths in the lesion study — At the four-week testing point, two vehicle rats and four DNSP-11 rats died within hours of the d-amphetamine injection used to measure turning. The authors attribute it to a build-up effect of the repeated isoflurane anesthesia used for nasal dosing on top of the 6-OHDA lesion, note that the d-amphetamine dose is not known to cause such losses, and caution other investigators about repeated isoflurane for this procedure (Stenslik et al., 2015).
• What the dopamine findings could cut both ways — The monkey study’s result was a fall in dopamine metabolites and turnover ratios on the unlesioned side, read by its authors as normalization but a suppression on the numbers, and suppression of dopamine and its metabolites has also been seen at higher doses of GDNF in monkeys and rats (Stenslik et al., 2018). In rats, the 1,000 µg nasal dose worked less well than 300 µg (Stenslik et al., 2015).
• Where the sequence appears in the body — The same 11 amino acids, or sequences close to them, are found in the locus ceruleus and other monoamine nuclei of the rat brain, in neuropeptide Y, which shares five consecutive residues, and in the TRK-fused gene product (Sonne et al., 2019). What a peptide given from outside does in those systems has not been tested.
• Not tested at all — No reproductive, genotoxicity or chronic-toxicity study, no drug-interaction study and no study in a person of any age turned up on PubMed or Europe PMC (searched October 4, 2026). The longest exposure on record is 10 weeks, in three monkeys (Stenslik et al., 2018).
• WADA — DNSP-11 is not named on the 2026 Prohibited List, and section S2.3 reaches growth factors "affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching"; DNSP-11 was studied on dopamine neurons, not on those tissues. Section S0 prohibits at all times any substance not addressed elsewhere on the List "with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued…)" (World Anti-Doping Agency, 2026). No approval of DNSP-11 anywhere turned up for this page, so it is prohibited at all times: under S0, or under S2.3 if WADA treats it as a growth factor modulator.

Bloodwork & Monitoring

No monitoring guidance for DNSP-11 exists, because no person has been given it and no trial has been registered (ClinicalTrials.gov, searched October 4, 2026). The animal studies measured these:

• Dopamine and its metabolites in tissue — Dopamine, DOPAC and homovanillic acid measured by HPLC with electrochemical detection in striatal and nigral tissue punches, and as the turnover ratio (DOPAC + HVA)/dopamine (Stenslik et al., 2015; Stenslik et al., 2018).
• Dopamine release in a living brain — Resting and evoked dopamine by microdialysis in the striatum, and potassium-evoked release by high-speed chronoamperometry at 500 µm steps through the striatum (Bradley et al., 2010; Fuqua et al., 2014).
• Behaviour — Apomorphine-induced and d-amphetamine-induced turning in lesioned rats, and distance travelled and movement speed in normal rats (Bradley et al., 2010; Fuqua et al., 2014; Stenslik et al., 2015).
• Cell counts and distribution — Tyrosine-hydroxylase-positive neuron counts and fibre density in the substantia nigra, and radioiodinated R9K peptide counted in brain sections, cerebrospinal fluid, blood and urine (Stenslik et al., 2015; Stenslik et al., 2018).
• In the monkeys — Body weight each dosing week and daily cage-side observation for nosebleeds, gastrointestinal signs and neurological events (Stenslik et al., 2018). No blood chemistry, blood count or organ-function panel is reported in the published studies.
• Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

Nothing, on the record. In every study DNSP-11 was given alone, against its vehicle or against a scrambled peptide of the same amino acids (Bradley et al., 2010; Fuqua et al., 2014; Stenslik et al., 2015); the monkeys had received MPTP months earlier, as the lesion, not as a co-treatment (Stenslik et al., 2018). The only published combination is a test tube: circular dichroism of DNSP-11 mixed with its siblings DNSP-5 and DNSP-17 matched the sum of the three separate spectra, which the authors read as showing the three act independently in vitro (Kelps et al., 2011). No study pairs DNSP-11 with any compound on this site, and no seller, clinic or guide describing such a pairing turned up (PubMed, Europe PMC and web searches, October 4, 2026), so this page carries no stack cards.

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Legal Status

Related Compounds

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Next Steps

References

1. UniProt Consortium. UniProtKB P39905 (GDNF_HUMAN), glial cell line-derived neurotrophic factor, Homo sapiens: 211 amino acids, with the sequence PPEAPAEDRSL at positions 28–38. rest.uniprot.org/uniprotkb/P39905.fasta. Read October 4, 2026.
2. Lin LF, Doherty DH, Lile JD, Bektesh S, et al. GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons. Science. 1993;260(5111):1130-1132. PMID: 8493557.
3. Immonen T, Alakuijala A, Hytönen M, Sainio K, et al. A proGDNF-related peptide BEP increases synaptic excitation in rat hippocampus. Exp Neurol. 2008;210(2):793-796. PMID: 18280470.
4. Bradley LH, Fuqua J, Richardson A, Turchan-Cholewo J, et al. Dopamine neuron stimulating actions of a GDNF propeptide. PLoS One. 2010;5(3):e9752. PMID: 20305789. (Full text at PMC2841203, read October 4, 2026: the DNSP-11 sequence PPEAPAEDRSL-amide, the 30 µg and 100 µg rat doses, the microdialysis and tissue figures, the pull-down table and the GFRα1 binding tests.)
5. Kelps KA, Turchan-Cholewo J, Hascup ER, Taylor TL, et al. Evaluation of the physical and in vitro protective activity of three synthetic peptides derived from the pro- and mature GDNF sequence. Neuropeptides. 2011;45(3):213-218. PMID: 21507484. (Full text at PMC3091812, read October 4, 2026: Table 1 gives DNSP-11’s calculated molecular weight 1,180, measured 1,180.3 after 31 days at 37 °C and 97.6% remaining at 30 days; DNSP-5 542 and DNSP-17 1,868.)
6. Littrell OM, Fuqua JL, Richardson AD, Turchan-Cholewo J, et al. A synthetic five amino acid propeptide increases dopamine neuron differentiation and neurochemical function. Neuropeptides. 2013;47(1):43-49. PMID: 22981157.
7. Fuqua JL, Littrell OM, Lundblad M, Turchan-Cholewo J, et al. Dynamic changes in dopamine neuron function after DNSP-11 treatment: effects in vivo and increased ERK 1/2 phosphorylation in vitro. Peptides. 2014;54:1-8. PMID: 24406899. (Full text at PMC3989369, read October 4, 2026: the scrambled control peptide, the chronoamperometry subregion results, the ERK1/2 figures and the conflict-of-interest statement naming four pending patents.)
8. Stenslik MJ, Potts LF, Sonne JW, Cass WA, et al. Methodology and effects of repeated intranasal delivery of DNSP-11 in a rat model of Parkinson’s disease. J Neurosci Methods. 2015;251:120-129. PMID: 25999268. (Full text at PMC4500736, read October 4, 2026: the dose-response, the lesion study, the tyrosine hydroxylase counts, the tracer study, the rat attrition after d-amphetamine and the rat plasma half-life given as data not shown.)
9. Stenslik MJ, Evans A, Pomerleau F, Weeks R, et al. Methodology and effects of repeated intranasal delivery of DNSP-11 in awake Rhesus macaques. J Neurosci Methods. 2018;303:30-40. PMID: 29614295. (Full text at PMC5965701, read October 4, 2026: six female macaques, three on DNSP-11, the 0.3–10 mg dose escalation over 10 weeks, the neurochemical results and the disclosure of two awarded and two pending patents.)
10. Sonne JWH, Groshong JS, Seavey C, Gash DM. Spatial and temporal immunoreactivity in the rat brain using an affinity purified polyclonal antibody to DNSP-11. J Chem Neuroanat. 2019;100:101664. PMID: 31394198. (Full text at PMC6745710, read October 4, 2026: the rat numbers, the locus ceruleus signal and the neuropeptide Y and TRK-fused gene product sequence homologies.)
11. Liu QR, Zhu M, Chen Q, Mustapic M, et al. Novel Hominid-Specific IAPP Isoforms: Potential Biomarkers of Early Alzheimer’s Disease and Inhibitors of Amyloid Formation. Biomolecules. 2023;13(1):167. PMID: 36671553. (Full text at PMC9856209, read October 4, 2026: the Thioflavin T figures for DNSP-11 against IAPP37 and amyloid-β 42.)
12. Sidorova YA, Saarma M. Small Molecules and Peptides Targeting Glial Cell Line-Derived Neurotrophic Factor Receptors for the Treatment of Neurodegeneration. Int J Mol Sci. 2020;21(18):6575. PMID: 32911810.
13. Conway JA, Kramer ER. Is activation of GDNF/RET signaling the answer for successful treatment of Parkinson’s disease? A discussion of data from the culture dish to the clinic. Neural Regen Res. 2022;17(7):1462-1467. PMID: 34916419.
14. Wen P, Ren C. Research progress on intranasal treatment for Parkinson’s disease. Neuroprotection. 2024;2(2):79-99. PMID: 41383697.
15. Parshina VV, Revishchin AV, Pavlova GV. [Isoforms of glial cell line-derived neurotrophic factor and their therapeutic potential]. Zh Vopr Neirokhir Im N N Burdenko. 2025;89(6 Vyp 2):38-43. PMID: 41527797. (In Russian; English abstract read October 4, 2026.)
16. Atkinson EA, Liu T, Fowler M, Smith PO, et al. Peptides Targeting GDNF Family Receptor Alpha 1 (GFRα1) Mimic Glial Cell Line-Derived Neurotrophic Factor (GDNF) Bioactivity. J Med Chem. 2026;69(10):11914-11925. PMID: 42100797.
17. Gill SS, Patel NK, Hotton GR, O’Sullivan K, et al. Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinson disease. Nat Med. 2003;9(5):589-595. PMID: 12669033.
18. Slevin JT, Gerhardt GA, Smith CD, Gash DM, et al. Improvement of bilateral motor functions in patients with Parkinson disease through the unilateral intraputaminal infusion of glial cell line-derived neurotrophic factor. J Neurosurg. 2005;102(2):216-222. PMID: 15739547.
19. Lang AE, Gill S, Patel NK, Lozano A, et al. Randomized controlled trial of intraputamenal glial cell line-derived neurotrophic factor infusion in Parkinson disease. Ann Neurol. 2006;59(3):459-466. PMID: 16429411.
20. Whone A, Luz M, Boca M, Woolley M, et al. Randomized trial of intermittent intraputamenal glial cell line-derived neurotrophic factor in Parkinson’s disease. Brain. 2019;142(3):512-525. PMID: 30808022.
21. Bradley LH, Gash DM, Gerhardt GA. Amidated dopamine neuron stimulating peptide restoration of mitochondrial activity. US Patent 9,402,875 B2, granted August 2, 2016; assignee University of Kentucky Research Foundation; filed August 15, 2012; priority October 27, 2006; adjusted expiration February 11, 2028. patents.google.com/patent/US9402875B2/en. Read October 4, 2026.
22. Bradley L, Gash DM, Gerhardt GA. Amidated dopamine neuron stimulating peptides for CNS dopaminergic upregulation. US Patent 9,586,992 B2, granted March 7, 2017; assignee University of Kentucky Research Foundation; filed January 13, 2014; anticipated expiration October 26, 2027; claims cover administration in Parkinson’s disease, Alzheimer’s disease and ALS. patents.google.com/patent/US9586992B2/en. Read October 4, 2026.
23. Gash DM, Gerhardt GA, Glass JD. Amidated dopamine neuron stimulating peptides for CNS dopaminergic upregulation. International application PCT/US2007/022696, published as WO 2008/069876 A2 on June 12, 2008; applicant University of Kentucky Research Foundation; legal status recorded as ceased. patents.google.com/patent/WO2008069876A2/en. Read October 4, 2026.
24. FDA. Drugs@FDA through openFDA (api.fda.gov/drug/drugsfda.json) and the National Drug Code Directory (api.fda.gov/drug/ndc.json): searches for DNSP-11 and dopamine neuron stimulating peptide, October 4, 2026 (no records). European Medicines Agency. Medicines data table (medicines-output-medicines_json-report, 2,746 records, timestamp October 4, 2026): no entry for DNSP-11.
25. Code of Federal Regulations. 21 CFR 216.23, bulk drug substances that can be used to compound drug products under section 503A, and 216.24, drug products withdrawn or removed from the market. ecfr.gov. Read October 4, 2026.
26. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated May 14, 2026. fda.gov/media/94155/download.
27. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503B of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated March 21, 2025. fda.gov/media/94164/download.
28. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances; S2.3, Growth factors and growth factor modulators. wada-ama.org.
29. Searches of October 4, 2026: PubMed, "DNSP-11" and "DNSP11" (8 records each, the same ones), "dopamine neuron stimulating peptide" (1,118 records, of which the DNSP papers), "GDNF propeptide" (4 records), DNSP-11 with toxicology, pregnancy, drug-interaction and combination terms (no records), and DNSP-11 with each brain compound on this site (no records); Europe PMC, "DNSP-11" (14 records, exact phrase: the six primary papers, five reviews, three research papers); ClinicalTrials.gov, "DNSP-11" (no records) and "dopamine neuron stimulating peptide" (2 unrelated records); NIH Dietary Supplement Label Database, "DNSP-11" (no labels); fda.gov warning-letter search for DNSP-11 (no letters); a research-reagent catalogue listing DNSP-11 trifluoroacetate salt, 1 mg, and web searches for sellers of DNSP-11 for human use (none found; suppliers not named).

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