Peptide education
SHLP2
SHLP-2
SHLP2, short for small humanin-like peptide 2, is a 26-amino-acid peptide encoded in the mitochondrial 16S rRNA region, described in 2016 as part of the same mitochondrial peptide family as humanin and MOTS-c. In cells and mice it does interesting things: it protects cells under stress, improves insulin action, activates appetite-regulating neurons, and raises thermogenesis. The human record is a handful of biomarker and genetics studies, several of which point in opposite directions. No one has ever published a study of SHLP2 administered to a person.
SHLP2 is a 2016 discovery with good mouse data, contradictory human biomarker findings, and zero human dosing studies. Anything sold under its name is a research reagent wearing a longevity story.
Overview
Quick answer
The name SHLP2 can mean endogenous peptide biology, a laboratory research reagent, a vendor vial, or a gray-market listing. A biomarker paper can tell you whether SHLP2 tracks with a disease state; a rodent or cell study can test mechanism; a vendor vial only raises identity and quality questions. None of those sources provides a human therapeutic dosing record.
What is SHLP2?
A 26-amino-acid peptide reported from the mitochondrial 16S rRNA region, sequence MGVKFFTLSTRFFPSVQRAVPLWTNS, in the same mitochondrial-derived peptide family as humanin. It entered the literature in 2016, which makes it one of the newest entries in this market.
Why do people talk about it?
Because the preclinical record is genuinely active: cell survival, lower ROS, better insulin action in rats, reduced food intake and higher thermogenesis in mice, and protection in a Parkinson's mouse model. Sellers read that record as a weight-loss and longevity product; the literature only supports it as a research direction.
What human evidence exists?
Observations, not treatments. One study found higher circulating SHLP2 tracks with android and liver fat, a tiny male-only study found lower SHLP2 in obese and diabetic men, a prostate-cancer paper found subgroup associations, and a genetics paper linked a K4R variant to lower Parkinson's risk. None of them gave anyone SHLP2.
What route and exposure patterns are documented?
Only laboratory ones: infusion into rat brains, intraperitoneal injections in mice, micromolar concentrations in cell culture. There is no human route, dose, or schedule on record, and vendor listings do not change that.
What does the evidence establish?
That SHLP2 is a legitimate research target with unresolved biology, including a 2023 analysis questioning how well the peptide is even conserved across evolution. It does not establish that taking SHLP2 does anything in a person, helpful or harmful.
Reported practice
Commonly reported protocol
No established community protocol. Community-reported patterns, not verified by controlled human trials and not a use recommendation. Full use-pattern detail
Evidence
Evidence snapshot
Foundational cell and rodent studies reported cytoprotective, metabolic, mitochondrial, and inflammatory-marker effects. That explains why researchers study SHLP2, but it does not show that SHLP2 works as a treatment in people.
Human studies report associations in adiposity, obesity or diabetes, prostate-cancer risk, and Parkinson's-related mitochondrial genetics, but none tested SHLP2 as a treatment.
Mouse and cell findings are often stretched into anti-aging, weight-loss, glucose-control, Parkinson's, AMD, and performance claims that the human literature cannot carry.
SHLP2 appears in research-supplier and public online listings with purity or COA language. HPLC or mass-spec style paperwork still leaves sterile pharmaceutical release questions open.
Claims
Common claims vs evidence
| Claim | Human evidence | Mechanistic evidence | Anecdotal evidence | Verdict |
|---|---|---|---|---|
| SHLP2 is a human weight-loss peptide. | Human intervention trials are missing. Human metabolic data are biomarker-based and inconsistent: one study linked higher SHLP2 with android and liver fat, while another small male-only study found lower SHLP2 in obese and diabetic men. | Mouse work supports appetite, thermogenesis, glucose handling, POMC neuron activation, and CXCR7 signaling. That is a strong reason to study metabolism, but it is not a human weight-loss result. | Vendor and gray-market pages often repeat the obesity and metabolism theme, usually by borrowing from rodent and biomarker papers. | Not established as a human-use claim. The cited evidence is preclinical metabolism plus mixed human biomarker findings. |
| SHLP2 improves insulin sensitivity or glucose control. | The human studies are observational or cross-sectional, so they leave open whether SHLP2 treatment improves glucose control. | Foundational rat clamp work and mouse studies reported improved insulin action, glucose uptake, hepatic glucose production signals, and obesity-model physiology. | Online product descriptions often translate insulin and obesity-model findings into diabetes-support language. That is a bigger claim than the available SHLP2 evidence. | Supported as a preclinical research theme, not as a human diabetes or glucose-control therapy. |
| SHLP2 is a longevity or anti-aging peptide. | No lifespan trial or human anti-aging intervention study found. The cited sources note age-related decline in mice and broader mitochondria-derived peptide interest. | SHLP2 touches apoptosis, ROS, mitochondrial respiration, ATP, amyloid handling, inflammatory markers, and stress biology, which is why aging-related hypotheses appear in the literature. | Longevity language appears in peptide-market descriptions more easily than it appears in human outcomes. | Relevant to aging biology, but not evidence for a human longevity therapy. |
| SHLP2 treats Parkinson's disease. | The human evidence is genetic association, not treatment. The K4R variant paper linked mitochondrial SNP m.2158T>C with lower Parkinson's risk and then studied SHLP2 biology in models. | The Parkinson's paper reported greater K4R stability, mitochondrial inner membrane and complex I connections, and protective effects in model systems. | Neuroprotection language can travel quickly online because the mechanism is easy to overread, but no human treatment outcome was reported. | This is genetics and model-based neuroprotection research, not evidence for a Parkinson's treatment. |
| SHLP2 helps AMD or vision. | No patient treatment study found. The vision-related SHLP2 evidence in the available material is mostly retinal cell-model work and a conference-level plasma-fragment signal. | The AMD cybrid work reported mitochondrial and viability effects at 3.2 micromolar SHLP2 in culture, which supports a retinal mitochondrial research question. | Vendor disease lists can turn the retinal-cell model into broader vision language. | Cell-model interest only, not an AMD or vision treatment claim. |
| SHLP2 is clinically safe because it is endogenous. | Being endogenous still leaves therapeutic dose, route, half-life, immunogenicity, chronic exposure, reproductive risk, cancer risk, and drug interaction questions open. No human dosing safety data were found. | SHLP2 affects systems tied to central energy regulation, survival signaling, mitochondrial function, and proteostasis. That is enough to make safety questions more important, not less important. | Research-use listings and COA language may make a vial look simple, but they leave open sterile injectable quality or clinical suitability. | Exogenous SHLP2 product safety remains a major unknown. |
Bottom line
Main takeaway
SHLP2 is a real peptide with real mouse studies, no human dosing record at all, and human biomarker findings that contradict each other. Treat any product claim accordingly.
Compared with MOTS-c, which at least has a recruiting human trial, SHLP2 has never been given to a person in a published study. Price that gap before anything else.
The record runs Cobb 2016, Okada 2017, Sequeira 2021, Kim 2023, Kim 2024, and the Gruschus 2023 conservation critique, with vendor listings and FDA peptide-quality materials as market context. That is a preclinical file, not a clinical one.
Identity
What it is
SHLP2 is a 26-amino-acid peptide from the mitochondrial 16S rRNA region, part of the mitochondrial-derived peptide family alongside humanin and MOTS-c. It appeared in the literature in 2016.
The preclinical case is broad: cytoprotection with less apoptosis and ROS, improved insulin sensitivity in rat clamp studies, chaperone-like handling of misfolded IAPP, and a 2023 Nature Communications paper proposing that SHLP2 activates CXCR7 on hypothalamic POMC neurons to cut food intake and raise brown-fat thermogenesis. A 2024 paper tied a K4R variant to lower Parkinson's risk and stronger mitochondrial protection in models.
The human case is thin and self-contradictory. Higher circulating SHLP2 was linked to more android and liver fat in one cohort, while a small male-only comparison found lower SHLP2 in obese and diabetic men. Those cannot both be simple good-news stories, and neither says what an injection would do.
There is even a basic-biology caveat: a 2023 evolutionary analysis found weak conservation support for SHLP2 compared with humanin or SHLP6. None of this makes SHLP2 fake. It makes it early, and it makes every product sold under the name an extrapolation.
How people talk about it online
SHLP2 barely exists in clinic culture. Its market is research-supplier listings, institutional catalogs, and a few public sales pages with COA downloads, and that obscurity is itself information: even the peptide industry has not built a practice around it.
The claims on those pages echo the paper abstracts: metabolism, weight, glucose, neuroprotection, retinal disease, aging. That is the literature being resold, not an independent signal from users.
Research-use labeling and purity paperwork leave every practical question open: identity, aggregation, sterility, endotoxin, stability. For a peptide with no human dosing record, those are not fine print; they are the whole product question.
Use context
Routes, doses, and cycle patterns
The cited material does not provide a human treatment schedule for SHLP2. The concrete numbers in the research are laboratory and animal-study conditions: ICV infusion in rats, intraperitoneal injection in mice, acute and chronic mouse obesity models, cell-culture micromolar or nanomolar exposures, and vendor product sizes. These are study conditions and market context, not use instructions or a public dosing schedule.
Human studies and product labels
Rat central infusion clamp study
- Purpose
- Insulin responsiveness and glucose flux
- Context
- Foundational rodent metabolic experiment
- Route
- Intracerebroventricular infusion
- Amount
- 0.16 micrograms/kg/min
- Frequency
- Continuous during clamp study
- Duration
- Acute clamp experiment
This was a mechanistic rat study measuring insulin action, glucose infusion rate, hepatic glucose production, and peripheral glucose uptake. It is not a human regimen.
Mouse inflammatory and metabolic biomarker dosing
- Purpose
- Serum insulin, leptin, IL-6, MCP-1, and metabolic readouts
- Context
- Foundational mouse experiment
- Route
- Intraperitoneal
- Amount
- 2 mg/kg per dose
- Frequency
- Twice daily
- Duration
- 5 days
This schedule helps explain why metabolism and inflammatory-marker claims appear around SHLP2, but it remains a mouse experiment.
Diet-induced obesity mouse metabolomics
- Purpose
- Plasma metabolite profiling after SHLP2 exposure
- Context
- Mouse systems-metabolomics study
- Route
- Intraperitoneal
- Amount
- 2.5 mg/kg per injection
- Frequency
- Twice daily
- Duration
- 3 days
The study looked at pathway-level metabolomic changes after HNG or SHLP2 treatment in diet-induced obesity mice.
Obesity-model acute feeding and chronic HFD studies
- Purpose
- Food intake, thermogenesis, glucose handling, and obesity prevention
- Context
- Mouse obesity and CXCR7/POMC mechanism study
- Route
- Intraperitoneal and central experimental routes in mice
- Amount
- Acute effective dose reported as 2 mg/kg IP; ICV studies included 3 micrograms
- Frequency
- Acute dosing and daily injection in chronic experiments
- Duration
- Acute feeding tests and daily injection for 3 weeks in HFD-fed mice
This is the clearest metabolism paper, but the human component was a small serum comparison rather than a dosing trial.
AMD cybrid cell study
- Purpose
- Retinal mitochondrial and cell-viability readouts
- Context
- In vitro disease model
- Route
- Cell culture
- Amount
- 3.2 micromolar in culture media
- Frequency
- Laboratory exposure
- Duration
- Cell-culture context, not a human or animal dosing cycle
This supports retinal-cell biology work rather than an AMD treatment claim.
Cell-culture foundational assays
- Purpose
- Viability, apoptosis, oxygen consumption, ATP, ROS, and amyloid-beta toxicity
- Context
- Mechanistic cell studies
- Route
- Cell culture
- Amount
- Commonly 100 nM; cortical-neuron amyloid-beta work included 1 nM, 100 nM, and 10 micromolar
- Frequency
- Laboratory exposure
- Duration
- Cell-culture context, not a human or animal dosing cycle
These experiments explain the cytoprotective and mitochondrial language around SHLP2.
Parkinson's K4R SHLP2 mouse model
- Purpose
- Protection against toxin-induced dopaminergic injury
- Context
- MPTP mouse Parkinson's model
- Route
- Intraperitoneal
- Amount
- K4R SHLP2 2.5 mg/kg
- Frequency
- Twice daily in a pretreatment paradigm
- Duration
- Began 5 days before toxin challenge in the reported model
This is model evidence tied to a genetic association, not a human Parkinson's treatment regimen.
Newer cell-model expansions
- Purpose
- Oxidative-stress rescue and allergic-asthma-related preclinical work
- Context
- Cell and animal preclinical studies
- Route
- Cell culture or animal-model conditions
- Amount
- Pre-osteoblastic work used 10 micromolar, with some 5 micromolar comparator conditions
- Frequency
- Laboratory exposure
- Duration
- Not a clinical cycle
These newer papers show how SHLP2 claims are expanding into additional disease-model areas before human relevance is established.
Real-world discussion
No established community protocol
- Purpose
- Longevity discussion
- Context
- Research coverage only
- Route
- Not established
- Amount
- No consistent community range exists
- Frequency
- Not established
- Duration
- Not established
SHLP2 is an obscure mitochondrial-derived peptide with cell-level literature and no real-world use culture to speak of. There is no protocol to report, and any product sold under this name is unverified.
What varies
- Goal: mitochondrial biology, appetite, glucose handling, retinal-cell protection, Parkinson's-model protection, and longevity claims each require their own evidence.
- Human biomarker studies and human dosing trials answer different questions.
- Route: animal brain-infusion and intraperitoneal studies do not translate into a public human route.
- Amount: mg/kg animal doses and cell-culture concentrations are study conditions, not consumer regimens.
- Assay: the conflicting human metabolic findings may depend on population, sex, disease stage, assay method, peptide fragments, and sample size.
- Product quality: purity and mass confirmation still leave open whether an injectable product is sterile.
Human data
Human evidence
Every human SHLP2 datum is endogenous: measured in blood or read from genotype, never administered. The findings are a positive association with android and liver fat in people without diabetes, a tiny male-only serum study pointing the other direction in obesity and diabetes, a prostate-cancer biomarker subgroup analysis, a Parkinson's genetics association for the K4R variant, and detection of SHLP2 fragments in AMD plasma samples. No human dosing, pharmacokinetic, efficacy, or safety study exists in the cited record. The treatment question has simply never been tested in people.
Evidence maturity
SHLP2's evidence stops at preclinical biology and observational human biomarkers; every human-use claim is extrapolation.
Identified in 2016 as a mitochondria-derived peptide with cytoprotective and metabolic effects in cell and rodent experiments.
Mouse obesity, retinal-cell, and Parkinson's-model studies widened the claims, while a 2023 analysis questioned SHLP2's evolutionary conservation.
Observational studies linked circulating SHLP2 to fat distribution and a K4R variant to lower Parkinson's risk, but tested no treatment.
None exist for any claim; no human dosing, pharmacokinetic, efficacy, or safety study has been reported.
Vendor vials sell SHLP2 as research material whose COA paperwork cannot settle sterility or human suitability.
| Study / evidence area | Population | Design | Product context | Main outcome | Limitations | Weight |
|---|---|---|---|---|---|---|
| Android fat, liver fat, and metabolic syndrome associations | People without overt diabetes | Observational human biomarker study | Endogenous circulating SHLP2 measurement | Circulating SHLP2 was positively associated with multiple metabolic syndrome features, especially waist circumference, and with android and liver fat. | Association only. It leaves open whether giving SHLP2 would improve metabolism, and it conflicts directionally with the small obese/diabetic male serum comparison. | Limited human |
| Obesity and diabetes serum comparison | Healthy, obese, and diabetic men; groups reported as n=7, n=6, and n=7 | Small cross-sectional serum study | Endogenous SHLP2 measurement in a preclinical-heavy obesity paper | Serum SHLP2 was reported as lower in obese and diabetic men than in healthy men. | Very small, male-only groups with assay-method limitations. The finding leaves weight-loss and diabetes-treatment questions unanswered. | Weak human |
| Prostate-cancer biomarker association | Men undergoing prostate biopsy, with subgroup analyses by race | Biomarker association study | Endogenous SHLP2 biomarker, not SHLP2 treatment | Lower SHLP2 was linked with higher prostate-cancer risk in white men, with no significant association in black men and no association with grade in the citation record used here. | This is not a cancer prevention or treatment study, and the subgroup finding needs further study before clinical use. | Weak human |
| K4R SHLP2 and Parkinson's disease | Human mitochondrial SNP association cohorts with mechanistic follow-up | Genetics association plus cell and mouse model work | Endogenous variant biology and experimental SHLP2/K4R model exposure | mtSNP m.2158T>C, which changes SHLP2 to K4R, was associated with lower Parkinson's disease risk; model work tied SHLP2 to stability, mitochondrial complex I biology, and protection in experimental systems. | A protective variant association is about risk and model biology, not SHLP2 treatment in people. | Limited human genetics / preclinical |
| AMD plasma fragment analytical work | Human plasma samples in AMD-related analytical work | Conference abstract or analytical study | Endogenous or fragment detection, not therapeutic dosing | Degraded SHLP2 fragments, including oxidized fragments, were detected in AMD samples. | Preliminary analytical evidence. It offers no clinical benefit data or established diagnostic or treatment approach. | Preliminary human analytical |
Use context
Reported use context
The available details are animal and cell exposure conditions plus vendor product sizes, not a human protocol. Those laboratory conditions do not establish vendor product performance.
Study and label context
0.16 micrograms/kg/min during acute metabolic clamp work; animal study condition, not a human regimen.
2 mg/kg per dose twice daily for 5 days in one foundational mouse experiment; mouse study condition, not a human regimen.
Acute 2 mg/kg IP signal, 3 micrograms ICV in central experiments, and daily IP injection for 3 weeks in HFD-fed mice; preclinical metabolism research, not human dosing.
100 nM in several foundational assays, 3.2 micromolar in AMD cybrids, and 5 to 10 micromolar in newer pre-osteoblastic work; laboratory exposure conditions, not dosing guidance.
Real-world discussion
Institutional or public supplier pages listed SHLP2 in microgram or milligram quantities with purity or technical-document language; market and product documentation, not a treatment result.
Cautions
Safety and unknowns
- The cited evidence does not settle dose-related toxicity, tolerability, pharmacokinetics, half-life, tissue distribution, immunogenicity, reproductive safety, carcinogenicity, drug interactions, or long-term exposure risk for SHLP2 administration in people.
- Human metabolic biomarkers point in different directions across small studies. That makes simple claims such as "higher SHLP2 is always better" or "low SHLP2 causes metabolic disease" shaky.
- Much of the flagship metabolism work used male animals, and the small human obesity/diabetes comparison was male-only, so sex-specific effects still need study.
- Proposed activity in POMC neurons, CXCR7-MAPK/ERK signaling, brown-fat thermogenesis, survival signaling, and mitochondrial complex I biology is biologically active enough that human claims need safety data, not just mechanism diagrams.
- Cytoprotective and anti-apoptotic signaling may be useful in degenerative models, but it is not automatically benign across cancer contexts or chronic exposure.
- Posted purity, HPLC, MS, or COA snippets do not settle sterility, endotoxin, aggregation, peptide-related impurities, stability, potency, or whether a product matches the study material.
Product quality
A vial label is only a starting point
SHLP2 products look like research reagents or public online sales pages, not approved finished medicines. Some pages restrict access to institutional accounts; others show public sales language with "not for human use" disclaimers.
FDA peptide-quality materials emphasize impurity characterization, aggregation or oligomer state, physicochemical sameness, and biological activity. A purity percentage and mass match are useful starting points, but human-use confidence also requires impurity, sterility, endotoxin, stability, potency, and handling data.
Identity and sequence
SHLP2 claims depend on the exact peptide sequence and form. Strong identity work uses orthogonal methods, not only a vendor name.
Peptide content and assay
A vial label or purity percentage does not necessarily tell the actual active peptide content delivered after reconstitution or storage.
Impurities and aggregation
Peptide-related impurities, sequence variants, residuals, counterions, and aggregation can affect both activity and safety.
Sterility and endotoxin
Any injection use would require sterile-product controls and endotoxin testing, not just HPLC or mass-spec paperwork.
Stability and handling
Shipping temperature, lyophilized stability, reconstitution behavior, storage, and degradation products can change what a user actually has.
Mechanism
How it is proposed to work
SHLP2 appears to act as a mitochondrial and cellular stress-signaling peptide in experimental systems. The literature connects it with reduced apoptosis and ROS, higher oxygen consumption and ATP, insulin-action effects in rodents, amyloid-seed handling, hypothalamic appetite circuitry, CXCR7 signaling, thermogenesis, and mitochondrial complex I biology.
The 2016 foundational work reported increased cell viability, reduced apoptosis, lower ROS, higher oxygen consumption and ATP, ERK and STAT3 phosphorylation, and improved insulin action in rat clamp experiments.
A 2017 Scientific Reports paper proposed chaperone-like activity against misfolded, seeding-capable IAPP species, which gives SHLP2 a more specific proteostasis explanation than generic mitochondrial-support language.
The 2023 Nature Communications obesity paper proposed that SHLP2 binds and activates CXCR7, recruits beta-arrestin, activates ERK1/2 signaling, reaches cerebrospinal fluid after systemic injection in mice, activates hypothalamic POMC neurons, lowers food intake, and increases thermogenic signaling in brown adipose tissue.
The 2024 Molecular Psychiatry paper linked a K4R SHLP2 variant to greater peptide stability, mitochondrial inner membrane localization, complex I binding, and stronger protection in Parkinson's-related models.
The mechanistic caution is replication breadth. CXCR7, complex I, and conservation findings are important, but the clinical meaning still depends on human intervention studies.
SHLP2 is a small peptide encoded in the mitochondrial 16S rRNA region, part of the mitochondrial-derived-peptide family alongside MOTS-c and humanin. Early work links it to insulin-sensitivity and inflammatory signaling in cell and rodent models.
FAQ
Common questions
What is SHLP2?
SHLP2 is a mitochondrial-derived peptide with early cell and rodent metabolic literature. It is one of the more obscure entries in the mitochondrial-peptide family.
Does SHLP2 have human evidence?
None. The data are cell models and a small number of animal experiments.
Is there a community protocol?
No. SHLP2 has not developed any real-world use culture, and there is no protocol to report.
Details
Technical details
Sources
References
- 1.
Foundational SHLP2 biology. Cobb et al., 2016, Aging. Foundational SHLP biology, age-decline in mice, cell survival, ROS, OCR/ATP, central insulin-sensitization work.
- 2.
AMD cybrid cell study. Nashine et al., 2018, Scientific Reports. AMD cybrid in vitro rescue study, 3.2 µM SHLP2.
- 3.
DIO mouse metabolomics paper. Mehta et al., 2019, Metabolomics. DIO mouse metabolome after SHLP2 treatment.
- 4.
Obesity and CXCR7 paper. Kim et al., 2023, Nature Communications. Obesity-model physiology, human small serum study, POMC neurons, CXCR7 proposal.
- 5.
Prostate biomarker paper. Xiao et al., 2017, Oncotarget. Prostate cancer biomarker association.
- 6.
Parkinson's K4R paper. Kim et al., 2024, Molecular Psychiatry. K4R variant, Parkinson’s association, stability, complex I binding, MPTP model.
- 7.
SHLP2 conservation critique. Gruschus et al., 2023, Scientific Reports. Evolutionary selection analysis, SHLP2 conservation caution.
- 8.
MDP review. Miller et al., 2022, JCI review. MDP context, no lifespan experiments for SHLP2, comparison to humanin and MOTS-c, IP disclosures.
- 9.
SHLP patent sequence table. US20110039771A1 patent. Early SHLP definitions and SHLP2 sequence table.
- 10.
FDA peptide quality guidance. FDA synthetic peptide guidance. Quality and impurity expectations for peptides.
- 11.
FDA peptide immunogenicity material. FDA immunogenicity assessment material for generic peptides. Peptides can be immunogenic; quality attributes matter.
- 12.
FDA peptide marketing enforcement. FDA warning letters and FDA drug-risk pages relevant to research-use peptide marketing.
- 13.
FTC claim guidance. FTC health-products guidance. Health claims need truthful, non-misleading, science-backed substantiation.
- 14.
Phoenix Peptide listing. Phoenix Peptide SHLP2 listing. Institutional research-use market example.
- 15.
Supplier COA examples. Hello Bio / MedChemExpress COA-style market example. Public technical-doc visibility.
- 16.
Novoprolabs sale page. Novoprolabs SHLP2 public sale page and public COA example. Consumer-facing gray-market example.
- 17.
BioInfinityLab SHLP2 page. BioInfinityLab SHLP2 page. COA-verified and “not intended for human use” marketing pattern.
- 18.
Osteoblast stress model. Ryu et al., 2025, Scientific Reports. Pre-osteoblastic oxidative-stress model.
- 19.
Allergic-asthma model paper. Zhang et al., 2025, Cellular Signalling. Allergic-asthma preclinical expansion.
- 20.
AMD plasma-fragment abstract. Ghazaryan et al., 2023, IOVS abstract. Human plasma SHLP2 fragments in AMD-related analytical work.