CUPRIC CHLORIDE IN PLASTIC CONTAINER
Clinical safety rating: caution
Comprehensive clinical and safety monograph for CUPRIC CHLORIDE IN PLASTIC CONTAINER (CUPRIC CHLORIDE IN PLASTIC CONTAINER).
Copper is an essential trace element that serves as a cofactor for numerous enzymes, including cytochrome c oxidase, superoxide dismutase, ceruloplasmin, lysyl oxidase, and dopamine beta-hydroxylase. It is critical for mitochondrial respiration, antioxidant defense, connective tissue cross-linking, neurotransmitter synthesis, and iron homeostasis. Cupric chloride provides ionic copper for these physiological processes.
| Metabolism | Copper is absorbed in the stomach and proximal small intestine. It is transported bound to albumin and transcuprein, then primarily taken up by the liver. Hepatic copper is incorporated into ceruloplasmin or excreted into bile. Biliary excretion is the main route of elimination; minimal renal excretion occurs. No significant cytochrome P450 metabolism. |
| Excretion | Primarily renal; approximately 80% of absorbed copper is excreted in bile, with fecal loss accounting for the majority (about 80-90%) of total elimination. Urinary excretion is minimal (<5%) under normal conditions. |
| Half-life | Terminal elimination half-life of copper is approximately 2-4 weeks (13-28 days) in humans, reflecting slow turnover from tissue stores, particularly liver and brain. This long half-life is clinically important for cumulative toxicity risk. |
| Protein binding | Approximately 90-95% bound to serum proteins, primarily ceruloplasmin (85-90%), with small amounts bound to albumin, transcuprein, and other ligands. |
| Volume of Distribution | Vd approximately 0.3-0.5 L/kg, indicating distribution primarily into plasma and interstitial fluid, with some uptake into liver and other tissues. This relatively low Vd reflects extensive protein binding and limited extravascular distribution. |
| Bioavailability | Oral bioavailability of cupric chloride is variable, approximately 30-40%, due to incomplete absorption and first-pass hepatic extraction. Intravenous administration yields 100% bioavailability. |
| Onset of Action | Intravenous administration: Rapid distribution to tissues within minutes; clinical effects (e.g., correction of deficiency) may be observed within hours to days, but full normalization of copper-dependent enzymes can take weeks. |
| Duration of Action | Duration varies with dose and patient status; a single IV dose maintains adequate copper levels for about 24-48 hours in the blood, but tissue repletion persists for weeks. Clinical effects last as long as copper is available for enzymatic functions. |
0.5-2.5 mg copper per day intravenously as a supplement to parenteral nutrition.
| Dosage form | INJECTABLE |
| Renal impairment | No dose adjustment required for GFR ≥30 mL/min; for GFR <30 mL/min, monitor serum copper and adjust dose to avoid accumulation. |
| Liver impairment | No specific adjustment required; use with caution in severe hepatic impairment (Child-Pugh class C) due to impaired copper excretion. |
| Pediatric use | Neonates and infants: 20 mcg/kg/day intravenously; children: 20-50 mcg/kg/day intravenously, maximum 2.5 mg/day. |
| Geriatric use | No specific adjustment; use lowest effective dose and monitor renal function and copper levels due to age-related decline. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for CUPRIC CHLORIDE IN PLASTIC CONTAINER (CUPRIC CHLORIDE IN PLASTIC CONTAINER).
| Breastfeeding | Copper is excreted into breast milk, with average concentrations around 0.2-0.4 mg/L. The M/P ratio is approximately 0.1-0.2. Supplemental cupric chloride may increase milk copper levels but is generally considered compatible with breastfeeding at recommended dietary allowances. Caution with excessive doses. |
| Teratogenic Risk | Copper is an essential trace element required for fetal development. However, excessive copper can be teratogenic. Data on cupric chloride specifically is limited. In animal studies, high doses of copper have been associated with fetal malformations and developmental delays. In humans, deficiency is more common as a risk factor for neural tube defects, preterm birth, and low birth weight. No specific trimester risks are established for therapeutic doses. |
■ FDA Black Box Warning
None
| Serious Effects |
["Hypersensitivity to copper or any component of the formulation","Wilson disease (unless specifically indicated for deficiency under expert supervision)","Massive copper poisoning"]
| Precautions | ["Monitor copper levels to avoid toxicity, as excess copper can cause Wilson disease-like symptoms (hepatic necrosis, renal failure, hemolytic anemia).","Use with caution in patients with biliary obstruction (impaired copper excretion).","Aluminum toxicity risk: product may contain aluminum, which can accumulate in renal impairment.","Contains chloride; adjust electrolytes in patients with fluid/electrolyte disturbances."] |
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| Fetal Monitoring | Monitor maternal serum copper and ceruloplasmin levels, especially in Wilson's disease or long-term parenteral nutrition. Fetal monitoring includes ultrasound for growth and development if high doses are used. Liver function tests and hematological parameters should be followed for signs of copper toxicity or deficiency. |
| Fertility Effects | Copper is essential for reproductive function. Both deficiency and excess can impair fertility. In females, copper deficiency may cause anovulation; excess copper can be toxic to oocytes. In males, copper is required for spermatogenesis; imbalance can reduce sperm quality. Therapeutic use of cupric chloride is unlikely to impair fertility at recommended doses. |