Phocytan

Primary (accepted uses / purposes)

• Laboratory / research reagent: Used extensively in biochemical and enzymatic studies of carbohydrate metabolism (glycogen synthesis and glycogenolysis), enzyme assays (phosphoglucomutase, UDP-glucose pyrophosphorylase, glycogen synthase), and metabolic pathway mapping.
• Diagnostic & assay applications: Standard substrate or calibrator in in vitro diagnostic kits, enzymatic assays for glucose metabolism, and biochemical research protocols.
• Biotechnological applications: Feedstock or intermediate in in vitro enzymatic synthesis of activated sugar nucleotides (e.g., UDP-glucose) or in cell-free biosynthetic systems.
• Experimental / investigational: Rare, specialized experimental uses in animal studies examining carbohydrate metabolism, glycogen storage disorders, or as a research tool to probe metabolic flux. Not an approved therapeutic agent for human clinical use.

Clinically accepted off-label or experimental concepts

• Experimental infusion or perfusion studies (animal models) to transiently alter intracellular sugar-phosphate pools for mechanistic research.
• Use in ex vivo organ or tissue perfusion protocols to study glycogen metabolism or to support short-term energy requirements in isolated preparations.

Regulatory note: G1P is not approved for therapeutic use; any systemic administration to animals or humans is investigational and must follow institutional review, ethics approval, and specialist pharmacology guidance.

Common research/assay concentrations (non-systemic, illustrative):

• In vitro enzyme assays: Typical working concentrations range from low micromolar to low millimolar (e.g., 0.01–5.0 mM) depending on enzyme Km and assay design.
• Cell culture / ex vivo incubations: Often used at concentrations in the low-hundreds of micromolar to low millimolar range to modulate intracellular fluxes; exact concentration is experiment dependent.
• Animal experimental infusion (investigational): Published experimental protocols (animal models) use carefully titrated infusion rates designed to produce small, transient changes in tissue sugar-phosphate pools; these are specialist procedures and must be dose-calculated per body weight and monitored in real time for metabolic effects.

Routes of experimental administration:

• In vitro / ex vivo: added directly to assay buffers, culture medium, or perfusates.
• In vivo (research animals only): intravenous infusion or intraperitoneal injection in validated experimental protocols (not routine). Oral bioavailability of free G1P is limited because gut phosphatases and enzymes rapidly metabolize phosphorylated sugars.

Special populations / adjustments:

• There are no established therapeutic dosing regimens for pediatric, elderly, renal or hepatic impairment populations. Any experimental use in vulnerable populations requires specialist oversight and adjustment.

Administration notes for researchers:

• Prepare fresh working solutions in appropriate buffer; avoid prolonged storage of aqueous solutions at room temperature. Account for pH and ionic strength in assay buffers because phosphate groups affect ionic balance. Use sterile, endotoxin-free reagents for cell culture or in vivo work.

Glucose-1-phosphate is a phosphorylated monosaccharide that functions as a central metabolic intermediate linking glycogen metabolism and glycolysis/gluconeogenesis. At the cellular level, G1P is rapidly interconverted with glucose-6-phosphate by phosphoglucomutase; it is a direct precursor for UDP-glucose formation (via UDP-glucose pyrophosphorylase), which is the activated donor for glycogen synthesis (glycogenesis). Conversely, during glycogenolysis, glycogen phosphorylase yields G1P from glycogen. Thus, supplying G1P in an experimental system elevates the local pool of sugar-phosphate substrates, driving downstream enzymatic reactions involved in glycogen assembly or glycolytic flux, depending on cellular context and enzymatic activities present.

• Absorption: Phosphorylated sugars like G1P have poor oral bioavailability because intestinal phosphatases and transport mechanisms preferentially handle non-phosphorylated monosaccharides; systemic absorption following oral intake is negligible for intact G1P. In vitro and ex vivo applications bypass absorption concerns.
• Distribution: If introduced systemically (experimental animal infusion), G1P is expected to distribute into extracellular fluid and be rapidly transported into tissues where sugar-phosphate transporters and metabolic enzymes operate; however, free G1P is rapidly metabolized or dephosphorylated.
• Metabolism: Rapid enzymatic interconversion (G1P ↔ G6P) via phosphoglucomutase; G1P is consumed by UDP-glucose pyrophosphorylase to form UDP-glucose or may be dephosphorylated by phosphatases. It is integrated into central carbohydrate metabolism.
• Elimination: Not eliminated unchanged to any significant degree; metabolites (e.g., glucose, CO₂ via oxidation, glycogen storage) follow normal metabolic clearance pathways. Any small systemically absorbed G1P would be handled via intracellular metabolism rather than renal excretion of parent compound.
• Onset & duration: Intracellular effects are rapid — enzymatic conversion occurs on the timescale of seconds to minutes. Systemic presence, if experimentally induced, is short-lived due to rapid metabolism.

• Pregnancy: There is no established FDA pregnancy category for G1P because it is not a therapeutic drug. Systemic administration in pregnant humans is not an approved or established practice. In experimental animal studies, metabolic perturbation of phosphorylated sugar pools can affect fetal metabolism; therefore, avoid experimental systemic use in pregnancy unless justified by strong scientific rationale and approved by relevant regulatory/ethics bodies.
• Lactation: No clinical data; theoretical risk to infant from maternal systemic exposure is minimal because systemic administration is not routine and metabolic conversion is rapid. Use in lactating subjects is not standard and would be investigational.

• Primary class: Metabolic intermediate / biochemical reagent (not a therapeutic agent).
• Subclasses: Sugar-phosphate intermediate; glycogen/glycolysis pathway substrate.

• Not for clinical treatment: Do not use G1P as a substitute for approved metabolic therapies or nutritional glucose unless in ethically approved experimental protocols.
• Experimental contraindications: Avoid systemic administration in subjects with unstable metabolic control (e.g., uncontrolled diabetes, severe inborn errors of metabolism) unless specifically justified, because exogenous sugar-phosphate manipulation can perturb glucose homeostasis.
• Allergy/sensitivity: Pure G1P salts are chemically simple and allergic reactions are unlikely to the molecule itself; reactions are more commonly due to contaminants or formulation excipients—use high-purity, endotoxin-free preparations.

• Metabolic disturbance risk: Systemic or high local concentrations can rapidly alter intracellular sugar-phosphate pools, potentially causing transient hyperglycemia, shifts in ATP/ADP ratios, or altered glycogen metabolism. Monitor glucose and metabolic parameters in experimental in vivo use.
• Use only in controlled settings: In vivo administration should be limited to laboratory animal studies or highly controlled clinical research with ethics approval, appropriate monitoring (blood glucose, electrolytes, acid-base), and predefined stopping criteria.
• Contamination risks: Preparations for cell culture or in vivo use must be sterile and endotoxin-free to avoid confounding inflammatory responses.
• Not a nutritional replacement: G1P should not be used as a caloric or nutritional substitute in clinical nutrition without specialist oversight.

If used systemically in investigational contexts, possible effects include:

• Metabolic: Transient changes in blood glucose, potential hyperglycemia or reactive hypoglycemia depending on metabolic state and insulin response.
• Gastrointestinal: Nausea if administered orally as large amounts (though oral absorption is poor).
• Systemic: Rare, formulation-related reactions (infusion site irritation, hypersensitivity to impurities or excipients).
• Cellular toxicity: Very high intracellular sugar-phosphate levels can cause osmotic or metabolic stress in sensitive cell types in vitro—observe cells for viability.

Onset of adverse metabolic effects is rapid (minutes to hours) and is dose-dependent.

• Insulin and hypoglycemic agents: Co-administration with insulin or insulin secretagogues could modulate glycemic response to G1P; monitor glucose.
• Drugs altering carbohydrate metabolism: Agents that inhibit or induce phosphoglucomutase, glycogen phosphorylase, or enzymes of glycolysis/gluconeogenesis may change G1P fate and downstream effects.
• Metabolic modulators (e.g., glucocorticoids, catecholamines): These hormones alter glycogen/glycolytic flux and will affect how tissues handle exogenous G1P.
• Enzyme assay interference: In vitro presence of exogenous G1P can interfere with diagnostic enzymatic assays for glucose or glycogen metabolism unless accounted for in assay design.

• Research trend: Growing use of sugar-phosphate substrates in cell-free biosynthesis and synthetic biology to produce activated sugar nucleotides; G1P is a key precursor in enzymatic cascades for glycan synthesis.
• Clinical guideline status: No clinical treatment guidelines recommend systemic G1P administration; its use remains confined to laboratory, diagnostic, and investigational contexts.
• Regulatory note: Any in vivo human investigational use requires regulatory/ethics approval and appropriate preclinical toxicity data.

• Powder (recommended): store desiccated at -20°C or 4°C depending on supplier recommendations; protect from moisture and prolonged room-temperature exposure.
• Aqueous solutions / stock: prepare fresh; short-term storage at 4°C (hours to days) is common for sterile, buffered solutions; avoid repeated freeze-thaw cycles. For long-term storage, aliquot and freeze (-20°C or -80°C) if compatible with downstream use.
• pH & buffer considerations: G1P solutions are acidic due to the phosphate group; adjust buffer composition and ionic strength for biochemical compatibility.
• Handling: Use sterile, endotoxin-free solvents for biological work. Label with concentration, lot, date, and storage conditions. Dispose of unused solutions per institutional biosafety procedures.