Peptide Signalling Pathways Explained: GPCRs, cAMP, MAPK, PI3K–AKT and JAK–STAT in Molecular Research
Peptide Signalling Pathways: 7 Powerful Insights Into Cellular Communication
Peptide signalling pathways are molecular communication systems through which peptide-related signals influence cellular activity. They connect the recognition of a peptide ligand with changes in intracellular enzymes, second messengers, protein phosphorylation, gene expression and other measurable biological processes.
Many naturally occurring peptide hormones and neuropeptides communicate through receptors located on cell membranes. When an appropriate ligand interacts with its receptor, the receptor may undergo structural changes that influence proteins and enzymes inside the cell.
The resulting signal can involve several molecular steps rather than one direct reaction.
For example, activation of a G protein-coupled receptor may alter cyclic AMP concentrations, while activation of the insulin receptor can initiate phosphorylation events involving insulin receptor substrates and downstream kinases.
These mechanisms differ, even though both begin with extracellular molecular recognition.
Understanding peptide signalling pathways therefore requires distinguishing receptor activation from the intracellular events that follow.
A signalling response also depends on the biological system. The same receptor can produce different outcomes in different cell types because the available signalling proteins, regulatory mechanisms and gene-expression programmes are not necessarily identical.
Furthermore, a peptide may influence more than one intracellular pathway.
This creates opportunities for signalling cross-talk, feedback regulation and responses that change over time.
Researchers investigating peptide signalling pathways use biochemical, molecular and cell-based methods to determine which components participate in a response and whether the observed changes depend on a particular receptor or signalling mechanism.
This article examines seven important principles of intracellular peptide signalling, with particular attention to GPCRs, cyclic AMP, MAPK, PI3K–AKT, JAK–STAT and the experimental evidence needed to interpret pathway activation.
What Are Peptide Signalling Pathways?
Peptide signalling pathways are connected molecular processes that transmit or regulate signals associated with peptide ligands and their biological targets.
A typical receptor-mediated signalling process may involve four broad stages:
- A peptide ligand interacts with a compatible receptor.
- The receptor undergoes a functional change.
- Intracellular signalling molecules respond.
- The cell produces a measurable biochemical or functional outcome.
However, this simplified sequence does not describe every peptide-related interaction.
Some peptides influence enzymes, membranes or other molecular targets without acting through conventional signalling receptors.
Additionally, intracellular pathways form networks rather than isolated linear chains.
One activated protein may influence several downstream molecules, and the same signalling protein may participate in responses initiated by different receptors.
Signal Transduction
Signal transduction describes the conversion and transmission of molecular information through a biological system.
In receptor-mediated peptide signalling pathways, signal transduction often involves protein interactions, enzymatic activity and changes in the concentrations of intracellular messengers.
Why Signalling Context Matters
A pathway may be present in several cell types but perform different functions depending on receptor expression, cellular state and interactions with other signalling networks.
Consequently, observing pathway activation does not independently establish a specific physiological or clinical outcome.
1. GPCR Signalling Connects Peptide Receptors to Intracellular G Proteins
G protein-coupled receptors, or GPCRs, form one of the largest receptor families involved in cellular communication.
Many peptide hormones and neuropeptides act through GPCRs.
Examples include GLP-1, glucagon and ghrelin receptor systems.
These receptors contain seven membrane-spanning helices and can influence intracellular heterotrimeric G proteins.
How GPCR Activation Begins
When a suitable ligand activates a GPCR, the receptor can promote nucleotide exchange on an associated G protein.
This process changes the activity of G protein components, allowing them to influence downstream effectors.
Different G protein families can produce different signalling outcomes.
Gs Signalling
Gs-associated signalling commonly stimulates adenylyl cyclase, an enzyme involved in cyclic AMP production.
Gi/o Signalling
Gi-associated signalling can inhibit certain adenylyl cyclase activities and influence additional effectors.
Gq/11 Signalling
Gq-associated signalling commonly activates phospholipase Cβ, which can generate intracellular signalling molecules involved in calcium mobilisation and protein kinase C regulation.
G12/13 Signalling
G12/13-associated pathways can influence Rho-family signalling and cytoskeletal regulation.
Why GPCR Signalling Is Not Uniform
A receptor’s signalling behaviour depends on its molecular characteristics, ligand, associated proteins and cellular environment.
Some receptors can interact with more than one G protein family.
Others participate in arrestin-associated signalling or intracellular trafficking processes.
Research on peptide signalling pathways therefore examines which signalling components are actually engaged rather than assuming that all GPCRs behave identically.
For related receptor biology, read Peptide Receptors Explained.
2. Cyclic AMP Acts as an Intracellular Second Messenger
Cyclic adenosine monophosphate, usually abbreviated as cAMP, is an intracellular second messenger.
It participates in many signalling systems, including those associated with certain peptide-activated GPCRs.
How cAMP Is Produced
Adenylyl cyclases catalyse the conversion of ATP into cAMP.
The activity of particular adenylyl cyclases can be influenced by G proteins and other regulatory mechanisms.
Protein Kinase A
One important downstream target of cAMP is protein kinase A, or PKA.
When activated, PKA can phosphorylate selected proteins and influence cellular processes.
CREB Signalling
The cAMP response element-binding protein, or CREB, is a transcription factor whose activity can be influenced by phosphorylation and other regulatory events.
CREB-associated transcriptional responses depend on the cellular context and the broader signalling environment.
EPAC Proteins
cAMP can also regulate exchange proteins directly activated by cAMP, commonly called EPAC proteins.
These provide an additional route through which cAMP can influence cellular activity.
Signal Termination
Phosphodiesterases degrade cyclic nucleotides and help regulate cAMP concentrations.
Feedback mechanisms and receptor regulation also influence the duration of signalling.
Important Interpretation
An increase in cAMP does not automatically establish a particular downstream biological effect.
The response depends on which cAMP-sensitive proteins are present and how the cell integrates their activity.
This is why peptide signalling pathways should be studied at more than one molecular level.
3. MAPK Signalling Transmits Signals Through Protein Kinase Cascades
Mitogen-activated protein kinase signalling, commonly abbreviated as MAPK signalling, involves interconnected kinase cascades.
These pathways participate in many cellular processes, including responses to extracellular signals, stress and changes in the cellular environment.
MAPK signalling can be influenced by several receptor families, including certain GPCRs and receptor tyrosine kinases.
The RAF–MEK–ERK Cascade
One well-characterised pathway involves sequential activation of RAF, MEK and ERK proteins.
A simplified representation is:
Receptor-associated signalling → RAS → RAF → MEK → ERK
This is not a universal pathway sequence for every receptor or cell type.
ERK Signalling
Extracellular signal-regulated kinases, or ERKs, can phosphorylate multiple cellular targets.
Depending on the system, ERK signalling may influence transcriptional regulation, protein activity and other cellular responses.
Other MAPK Families
MAPK signalling also includes pathways involving p38 MAPKs and c-Jun N-terminal kinases, commonly called JNKs.
These pathways have overlapping and distinct regulatory functions.
Why Phosphorylation Matters
Protein phosphorylation can change enzyme activity, molecular interactions, localisation or stability.
However, a phosphorylation event must be interpreted in relation to the specific protein, site and biological context.
Experimental Limitation
An increase in phosphorylated ERK is evidence of a change in the measured phosphorylation state.
It does not automatically establish increased cell proliferation, improved tissue function or any other particular biological outcome.
Research involving peptide signalling pathways must distinguish a biochemical marker from the broader process it may help regulate.
4. PI3K–AKT Signalling Integrates Metabolic and Cellular Signals
The phosphoinositide 3-kinase–AKT pathway, commonly called PI3K–AKT, is another major intracellular signalling system.
It participates in the regulation of metabolism, protein activity and cellular responses.
Insulin receptor signalling is an established example of a biological system that can engage PI3K–AKT.
Receptor Activation
The insulin receptor possesses intrinsic tyrosine kinase activity.
Following appropriate ligand binding, receptor activation can initiate phosphorylation events involving insulin receptor substrates.
PI3K Activation
PI3K enzymes can generate phosphoinositide lipid signals that recruit selected signalling proteins to cellular membranes.
AKT Activation
AKT, also known as protein kinase B, is regulated through phosphorylation and associated molecular interactions.
Activated AKT can influence multiple downstream targets.
mTOR-Associated Signalling
AKT signalling can interact with regulatory systems involving mechanistic target of rapamycin, or mTOR.
However, the relationship is complex and depends on cellular conditions.
Why the Pathway Is Context-Dependent
The PI3K–AKT network contains feedback loops, regulatory phosphatases and interactions with other signalling systems.
A change in AKT phosphorylation does not establish that every downstream target has changed in the same direction.
Important Distinction
The presence of PI3K–AKT signalling in a biological process does not mean that every peptide influencing this pathway produces the same physiological response.
Understanding peptide signalling pathways requires evaluating the particular receptor, cell model and measured endpoint.
5. JAK–STAT Signalling Links Receptor Activation With Transcriptional Responses
The Janus kinase–signal transducer and activator of transcription pathway, known as JAK–STAT, is associated with several cytokine and hormone receptor systems. peptide signalling pathways
Growth hormone receptor signalling is a well-established example.
Unlike receptor tyrosine kinases, certain cytokine receptor family members do not possess intrinsic kinase activity.
Instead, they interact with associated intracellular kinases.
JAK Activation
Appropriate receptor activation can influence associated Janus kinases.
These kinases participate in phosphorylation events involving receptor-associated proteins and downstream targets.
STAT Proteins
STAT proteins can become phosphorylated in response to particular signalling events.
Depending on the STAT protein and cellular context, phosphorylation may contribute to dimerisation, nuclear localisation and regulation of gene transcription. peptide signalling pathways
Growth Hormone Signalling
Growth hormone receptor activation can engage JAK2–STAT5-associated signalling.
However, growth hormone-related biological responses are not limited to one signalling pathway.
Feedback Regulation
Suppressor of cytokine signalling proteins, commonly called SOCS proteins, participate in feedback regulation of selected JAK–STAT systems.
Experimental Interpretation
Detecting phosphorylated STAT5 may support the presence of a signalling response under defined conditions.
It does not independently establish changes in tissue growth, strength or other complex outcomes.
Why This Matters
Research on peptide signalling pathways should identify the particular STAT protein, phosphorylation site, cell type and experimental conditions.
The phrase JAK–STAT activation alone may be too broad to describe the result accurately.
Comparing Major Peptide Signalling Pathways
The following table summarises several important systems.
| Signalling system | Example receptor context | Major molecular components | Common research measurements |
|---|---|---|---|
| GPCR–Gs | GLP-1 receptor | Gs, adenylyl cyclase | cAMP production |
| GPCR–Gq | Selected peptide-activated GPCRs | Gq, phospholipase Cβ | Calcium mobilisation, IP-related signals |
| MAPK–ERK | Multiple receptor families | RAS, RAF, MEK, ERK | ERK phosphorylation |
| PI3K–AKT | Insulin receptor | IRS proteins, PI3K, AKT | AKT phosphorylation |
| JAK–STAT | Growth hormone receptor | JAK2, STAT proteins | STAT phosphorylation, transcriptional responses |
These pathways are not mutually exclusive.
A single receptor may influence several networks, while different receptors may converge on some of the same intracellular proteins.
The table identifies representative mechanisms rather than complete descriptions of every pathway.
6. Signalling Cross-Talk and Feedback Change Cellular Responses
Biological signalling networks contain numerous connections between pathways.
This phenomenon is often called signalling cross-talk.
Cross-talk occurs when components of one signalling system influence another.
Shared Molecular Components
Different receptors may activate common intracellular kinases or second messengers.
Feedback Inhibition
A downstream response may reduce activity earlier in the pathway.
Feedback Amplification
Some regulatory mechanisms can increase or prolong selected signalling responses.
Receptor Regulation
Desensitisation, internalisation and changes in receptor availability can alter subsequent signalling.
Phosphatase Activity
Protein phosphatases remove phosphate groups from selected proteins and participate in signalling regulation.
Why Timing Matters
A pathway may show strong activation shortly after stimulation and reduced activity later.
This pattern may reflect feedback, receptor regulation or changes in the cellular environment.
Experimental Implications
Measuring one time point may provide an incomplete description of the signalling response.
Researchers studying peptide signalling pathways often need to consider how signals change over time.
For example, an early phosphorylation event and a later transcriptional response may not follow identical time courses.
These differences should not automatically be treated as contradictory. peptide signalling pathways
7. Experimental Evidence Determines What a Signalling Result Means
The final principle concerns the interpretation of laboratory findings.
A signalling pathway is a mechanistic framework, but an experiment measures particular molecular events.
The strength of the conclusion depends on what was actually observed.
Receptor Binding Assays
These measure ligand interactions with molecular targets.
They do not independently establish downstream signalling.
Second-Messenger Assays
These may measure cAMP, calcium or other intracellular signals.
They provide evidence about selected signalling processes.
Phosphorylation Assays
Western blotting, immunoassays and other methods may measure the phosphorylation state of specific proteins.
Gene-Expression Studies
RNA-based methods can examine changes in transcript abundance.
However, transcript changes do not always correspond directly to protein abundance or activity.
Protein Analysis
Proteomic methods and targeted protein assays can provide additional information about molecular responses.
Functional Cell Assays
These assess cellular outcomes such as changes in metabolic activity, movement or other measurable processes.
Why Multiple Measurements Help
A receptor-binding result, a phosphorylation result and a cellular functional result provide different types of evidence.
When interpreted together, they may support a more detailed mechanistic explanation.
Understanding peptide signalling pathways requires recognising these distinctions and avoiding conclusions that exceed the data. peptide signalling pathways
Worked Example 1: Interpreting a cAMP Concentration–Response Experiment
Consider a hypothetical peptide ligand tested in a cell model expressing a particular GPCR.
The laboratory measures intracellular cAMP relative to a baseline condition.
| Peptide concentration | Hypothetical cAMP response |
|---|---|
| 0 nM | 100% |
| 0.1 nM | 112% |
| 1 nM | 145% |
| 10 nM | 220% |
| 100 nM | 235% |
All values are illustrative.
Observation
The measured cAMP response increases across the concentration range and approaches a plateau.
Supported Interpretation
The results are consistent with a concentration-dependent change in intracellular cAMP under the stated assay conditions. peptide signalling pathways
What Cannot Be Concluded?
The data alone do not prove that the response is mediated exclusively by one receptor.
They also do not establish changes in gene expression or a clinical outcome.
Additional Evidence
Appropriate receptor controls, pharmacological tools or molecular methods may help investigate the mechanism.
Key Lesson
Peptide signalling pathways should be interpreted using the actual measured endpoint rather than assuming that one response establishes an entire downstream mechanism. peptide signalling pathways
Worked Example 2: Why Phosphorylation Does Not Equal Biological Efficacy
Consider a fictional study measuring ERK phosphorylation after peptide exposure.
| Time after exposure | Relative phosphorylated ERK |
|---|---|
| Baseline | 1.0 |
| 5 minutes | 2.8 |
| 15 minutes | 3.5 |
| 30 minutes | 1.9 |
| 60 minutes | 1.1 |
Values are hypothetical relative measurements.
Observation
ERK phosphorylation increases transiently and then approaches baseline.
Supported Interpretation
The experiment demonstrates a time-dependent change in the measured ERK phosphorylation signal.
What Cannot Be Concluded?
The results do not independently establish cell proliferation, tissue regeneration or any other complex biological outcome.
Why the Distinction Matters
ERK signalling participates in numerous cellular processes.
Its significance depends on the broader molecular and experimental context.
Key Lesson
An observed change in one component of peptide signalling pathways is not sufficient evidence for every process associated with that pathway. peptide signalling pathways
Worked Example 3: Two Peptides, Different Pathway Responses
Consider two hypothetical peptides tested in the same cell model.
The laboratory measures cAMP and phosphorylated ERK under defined conditions.
| Measurement | Peptide A | Peptide B |
|---|---|---|
| cAMP response relative to baseline | 240% | 130% |
| Phosphorylated ERK relative to baseline | 1.4-fold | 2.6-fold |
| Cell viability under assay conditions | No measured reduction | No measured reduction |
These results are fictional.
Initial Interpretation
Peptide A produces a larger cAMP response.
Peptide B produces a larger measured ERK phosphorylation response.
Does This Prove Biased Agonism?
No.
Formal assessment of signalling bias requires appropriate concentration–response analysis, a reference ligand and consideration of system-dependent factors.
What Can Be Concluded?
The two peptides demonstrate different response patterns in the selected assays.
Key Lesson
Research on peptide signalling pathways should distinguish descriptive pathway differences from formally established signalling bias.
Signal Amplification and Why Small Inputs Can Produce Large Responses
Some signalling systems amplify molecular information.
One activated receptor may influence multiple downstream proteins, which can in turn affect additional molecules.
This can produce a measurable response even when only a fraction of available receptors is occupied.
However, the degree of amplification depends on the receptor and cell system. peptide signalling pathways
Receptor Reserve
In some experimental systems, a maximal response can occur without occupancy of every receptor.
This phenomenon is associated with the concept of receptor reserve.
Implications for Potency
Functional potency may differ from binding affinity because signalling amplification influences the relationship between receptor occupancy and response.
Important Limitation
Amplification does not imply that a peptide will produce a large physiological effect in every biological system.
The relevant outcome must be measured directly.
This distinction is essential when interpreting peptide signalling pathways in molecular pharmacology.
Why the Same Peptide Can Produce Different Responses in Different Cells
The biological response to a peptide depends on more than its chemical structure.
Different cells may express different receptor quantities, signalling proteins, regulatory enzymes and transcription factors.
Receptor Expression
A cell with little or no relevant receptor expression may respond differently from a cell with substantial receptor expression.
Downstream Protein Availability
Cells vary in the abundance and activity of signalling proteins.
Feedback Regulation
Different cell types may possess different regulatory mechanisms.
Cellular State
Nutrient availability, differentiation state and other conditions may influence signalling.
Experimental Conditions
Assay duration, culture conditions and measurement methods can affect observed results.
Therefore, peptide signalling pathways should not be interpreted as producing one fixed response across every biological system.
How to Evaluate a Peptide Signalling Study
A useful scientific review begins with the experimental question.
The following checklist helps identify what a signalling study actually demonstrates.
| Review question | Why it matters |
|---|---|
| Was the peptide identity appropriately characterised? | Supports confidence in the tested material |
| Was the receptor or molecular target identified? | Clarifies the proposed mechanism |
| Was a suitable control included? | Supports interpretation of observed changes |
| Was a concentration–response relationship examined? | Helps characterise response behaviour |
| Were relevant time points measured? | Captures temporal changes |
| Was pathway specificity assessed? | Helps distinguish direct and indirect effects |
| Were measurements replicated? | Supports reproducibility |
| Were alternative explanations considered? | Reduces overinterpretation |
| Were functional outcomes measured separately? | Distinguishes signalling markers from biological effects |
| Were conclusions limited to the model studied? | Prevents unsupported generalisation |
Analytical material quality also matters.
A peptide sample containing unexpected impurities or undergoing degradation during an experiment can complicate interpretation.
For background on analytical characterisation, see Peptide Quality Control Checklist and Peptide Stability Testing.
Common Misconceptions About Peptide Signalling Pathways
1. Every Peptide Activates a Receptor
Some peptides interact with enzymes, membranes or other molecular targets.
2. All GPCRs Use the Same Signalling Pathway
Different GPCRs can engage different G proteins and regulatory mechanisms.
3. cAMP Activation Always Produces the Same Biological Effect
The outcome depends on cellular context and downstream signalling components.
4. Increased ERK Phosphorylation Proves Increased Cell Growth
ERK phosphorylation is a biochemical measurement, not direct proof of a complex cellular outcome.
5. PI3K–AKT Activation Automatically Establishes a Metabolic Benefit
A pathway measurement does not independently establish physiological or clinical efficacy.
6. JAK–STAT Signalling Is Identical in Every Cell Type
Receptor expression, STAT proteins and regulatory mechanisms vary.
7. One Signalling Assay Can Establish a Complete Mechanism
Different assays measure different molecular events.
8. Pathway Activation in Cultured Cells Proves a Human Outcome
Cellular findings cannot automatically be translated into clinical conclusions. peptide signalling pathways
These distinctions are essential for interpreting peptide signalling pathways accurately.
Frequently Asked Questions About Peptide Signalling Pathways
1. What are peptide signalling pathways?
Peptide signalling pathways are molecular systems through which peptide-related interactions influence intracellular signalling and measurable cellular responses.
2. How do peptide signalling pathways work?
Many begin with peptide binding to a receptor, followed by changes in intracellular proteins, second messengers or enzyme activity.
3. What is the role of GPCRs in peptide signalling?
GPCRs recognise many peptide ligands and can influence intracellular G proteins and downstream signalling networks.
4. What does cAMP do in peptide signalling?
cAMP acts as an intracellular second messenger that can regulate proteins such as PKA and EPAC.
5. What is the MAPK pathway?
MAPK pathways involve kinase cascades that transmit and regulate signals through phosphorylation events.
6. How is PI3K–AKT involved in peptide signalling?
PI3K–AKT participates in signalling associated with several receptor systems, including insulin receptor signalling.
7. What is JAK–STAT signalling?
JAK–STAT signalling involves receptor-associated kinases and STAT proteins that can influence transcriptional responses.
8. Can one peptide activate multiple signalling pathways?
Yes. Depending on the receptor and cell system, one peptide may influence several intracellular signalling networks.
9. How do researchers measure peptide signalling pathways?
Researchers use second-messenger assays, phosphorylation measurements, gene-expression studies and other molecular techniques.
10. Does activating a signalling pathway prove clinical effectiveness?
No. Pathway activation provides mechanistic evidence. Clinical outcomes require appropriate clinical research.
Conclusion: Understanding Peptide Signalling Pathways
Peptide signalling pathways connect molecular recognition with intracellular biochemical responses.
GPCR-associated signalling, cyclic AMP, MAPK, PI3K–AKT and JAK–STAT represent several important systems through which peptide-related signals can influence cellular activity.
However, these pathways do not operate as isolated or universally predictable chains.
Their behaviour depends on receptor identity, ligand characteristics, cellular context, feedback regulation and interactions with other signalling networks.
For researchers, the central challenge is determining what each experiment actually demonstrates.
A change in cAMP concentration is evidence about a second-messenger response. A phosphorylation measurement provides information about the state of a selected protein. A gene-expression change reveals another level of cellular regulation.
None of these measurements automatically establishes a clinical benefit.
Understanding peptide signalling pathways therefore requires integrating complementary experimental evidence while recognising the limits of each method.
This approach provides a stronger foundation for interpreting peptide-related molecular research and for distinguishing established mechanisms from hypotheses requiring further study.
Scientific References and Further Reading
- Rosenbaum, D. M., Rasmussen, S. G. F., Kobilka, B. K. (2009). The Structure and Function of G-Protein-Coupled Receptors. Nature, 459, 356–363.
https://doi.org/10.1038/nature08144 - Pierce, K. L., Premont, R. T., Lefkowitz, R. J. (2002). Seven-Transmembrane Receptors. Nature Reviews Molecular Cell Biology, 3, 639–650.
https://doi.org/10.1038/nrm908 - Lemmon, M. A., Schlessinger, J. (2010). Cell Signaling by Receptor Tyrosine Kinases. Cell, 141(7), 1117–1134.
https://doi.org/10.1016/j.cell.2010.06.011 - Manning, B. D., Toker, A. (2017). AKT/PKB Signaling: Navigating the Network. Cell, 169(3), 381–405.
https://doi.org/10.1016/j.cell.2017.04.001 - Cargnello, M., Roux, P. P. (2011). Activation and Function of the MAPKs and Their Substrates, the MAPK-Activated Protein Kinases. Microbiology and Molecular Biology Reviews, 75(1), 50–83.
https://doi.org/10.1128/MMBR.00031-10 - Rawlings, J. S., Rosler, K. M., Harrison, D. A. (2004). The JAK/STAT Signaling Pathway. Journal of Cell Science, 117, 1281–1283.
https://doi.org/10.1242/jcs.00963 - Beavo, J. A., Brunton, L. L. (2002). Cyclic Nucleotide Research — Still Expanding After Half a Century. Nature Reviews Molecular Cell Biology, 3, 710–718.
https://doi.org/10.1038/nrm911 - International Union of Basic and Clinical Pharmacology (IUPHAR). Guide to Pharmacology.
https://www.guidetopharmacology.org/ - National Center for Biotechnology Information (NCBI). PubMed Scientific Literature Database.
https://pubmed.ncbi.nlm.nih.gov/
These references provide foundational scientific context on receptor signalling and intracellular molecular pathways. They do not establish the activity, efficacy, safety or regulatory status of any particular commercial research peptide.
Research information notice: This article is intended for scientific education and laboratory research. All numerical examples are hypothetical and do not represent experimental results for Axion Peptide Lab products. Descriptions of molecular mechanisms are not claims of clinical benefit. Research peptides are not represented as suitable for human or veterinary administration.
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