Understanding the current situation and risk of environmental contamination by anti-influenza drugs in aquatic environments is key to prevent the unexpected emergence and spread of drug-resistant viruses. However, few reports have been focused on newer drugs that have recently been introduced in clinical settings. In this study, the behaviour of the prodrug baloxavir marboxil (BALM)-the active ingredient of Xofluza, an increasingly popular anti-influenza drug-and its pharmacologically active metabolite baloxavir (BAL) in the aquatic environment was evaluated. Additionally, their presence in urban rivers and a wastewater treatment plant (WWTP) in the Yodo River basin was investigated and compared with those of the major anti-influenza drugs used to date (favipiravir (FAV), peramivir (PER), laninamivir (LAN), and its active metabolite, laninamivir octanoate (LANO), oseltamivir (OSE), and its active metabolite, oseltamivir carboxylate (OSEC), and zanamivir (ZAN)) to comprehensively assess their environmental fate in the aquatic environment. The results clearly showed that BALM, FAV, and BAL were rapidly degraded through photolysis (2-h, 0.6-h, and 0.4-h half-lives, respectively), followed by LAN, which was gradually biodegraded (7-h half-life). In addition, BALM and BAL decreased by up to 47 % after 4 days and 34 % after 2 days of biodegradation in river water. However, the remaining conventional drugs, except for LANO (<1 % after 10 days), were persistent, being transported from the upstream to downstream sites. The LogK_d values for the rates of sorption of BALM (0.5-1.6) and BAL (1.8-3.1) on river sediment were higher than those of conventional drugs (-0.5 to 1.7). Notably, all anti-influenza drugs were effectively removed by ozonation (>90-99.9 % removal) after biological treatment at a WWTP. Thus, these findings suggest the importance of introducing ozonation to reduce pollution loads in rivers and the environmental risks associated with drug-resistant viruses in aquatic environments, thereby promoting safe river environments.

01 Oct 2024·PEDIATRICS

Severe Congenital Lead Poisoning in Siblings

Article

Author: Haile, Jennifer ; Velagala, Suganthinie ; Chhikara, Aditya

Congenital lead toxicity is rare. Lead freely crosses the placenta, therefore, placing the developing fetus at a higher risk for lead toxicity. This can lead to adverse consequences, such as spontaneous abortion, low birth weight, low IQ, and neurodevelopmental impairment. We present a rare case of siblings born to a mother with pica behaviors. Her venous lead level was 42 μg/dL at the time of disclosure. The repeat venous level at delivery 2 weeks later was 61 μg/dL. The infant’s venous level shortly after birth was 89 μg/dL. The neonate was transferred to the NICU, where he received 9 doses of intramuscular dimercaprol and 5 days of intravenous Ca2Na2EDTA. Seventy-two hours after completing chelation, the blood lead level rebounded to 46 μg/dL. A 19-day course of dimercaptosuccinic acid was then initiated. As of 12 months of age, he has not required additional chelation. Shortly after, the mother conceived another child, who was born prematurely at 29 weeks. Twelve days before delivery, the mother’s lead level was 30 ug/dL. The infant’s lead level was 32 ug/dL at the time of delivery. The infant’s lead trended down without requiring chelation. Both children have since demonstrated developmental delays and have needed early intervention services.

01 Oct 2024·The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG

Pediatric Lead Chelation Managed During Critical Medication Shortages: Case Report and Literature Review

Article

Author: Kane, Jason M. ; Said, Sana J. ; Singh, Mahi K.

Lead poisoning in children has the potential for devastating neurodevelopmental consequences. There is significant socioeconomic disparity in children with lead poisoning. Specific lead chelation regimens have been approved for children by the US Food and Drug Administration, however in the United States, there has been a recent national shortage of the primary therapy, edetate calcium disodium (CaNa2 EDTA). This case report presents a 23-month-old child with severe symptomatic lead poisoning during a national shortage of CaNa2 EDTA to highlight the need for advocacy regarding critical medication shortages, especially for antidote therapy. The infant’s initial blood lead level was 364 mcg/dL and he received a continuous infusion of CaNa2 EDTA (1000 mg/m2/day), as well as dimercaprol (4 mg/kg intramuscularly every 4 hours). The supply of CaNa2 EDTA was exhausted on day 3 of therapy so he was transitioned to enteral succimer monotherapy. Initial parenteral therapy of 72 hours achieved a lead level of 72 mcg/dL; he then completed his enteral course of succimer along with environmental mitigation. However, elevated blood lead levels persisted and he subsequently required 3 more courses of enteral succimer, and he continues to have detectable blood lead levels 2 years after initial presentation. In the face of medication shortages including CaNa2 EDTA, and now also dimercaprol, clinicians must create and study alternative chelation therapy regimens for pediatric lead toxicity. Furthermore, public policy initiatives, including the development of a national supply stockpile of chelation agents, must be created in order to minimize supply chain disruption and ensure adequate and equitable antidote therapy for lead poisoning outbreaks.

News (Medical) associated with Dimercaprol

13 Sep 2024

·www.biospace.com

Rising Pharmaceuticals announces commercial availability of Edetate calcium disodium injection in the United States

Rising’s Edetate calcium disodium injection is FDA-approved and immediately available Edetate calcium disodium injection is indicated for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. 1 EAST BRUNSWICK, N.J.--(BUSINESS WIRE)-- #adultleadpoisoning --Rising Pharma Holdings, Inc., d/b/a Rising Pharmaceuticals, Inc. (“Rising”) announced commercial availability of Edetate calcium disodium injection. Access to Rising’s product continues despite a commercial shortage of this product in the United States. Rising’s Edetate calcium disodium injection is indicated for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. “Rising’s Edetate calcium disodium injection provides an available option for health care providers to treat patients exposed to lead poisoning,” said David Picard, Executive Vice President for Institutional Markets at Rising. “This continued availability reflects our ongoing commitment to addressing product supply shortages to help ensure health care providers have access to products for patient care.” Edetate Calcium Disodium injection, USP 5 mL single-dose vial containing 200 mg of edetate calcium disodium per mL (1000 mg per vial) Supplied in boxes containing 5 vials (NDC 64980-588-51) Wholesale Item Numbers Cardinal 5855416 Cencora 10291753 Mckesson 2830826 Morris Dickson 296285 ___________________________ 1 Full prescribing information and label available at and provided below. About Rising Pharmaceuticals, Inc. Rising Pharmaceuticals, Inc. is a leading provider of generic and specialty-branded pharmaceuticals in the U.S. Rising focuses on the development, regulatory, and commercial aspects of the product life cycle while outsourcing manufacturing to its network of strategic CMO and CDO partners. With over 182 commercialized generic medicines and over 620 active SKUs, Rising has one of the largest portfolios of any generic pharmaceutical company in the US market. Through an extensive global network of manufacturing facilities, Rising supplies almost 9 billion doses of generic medicine to the market annually. The Company is based in New Brunswick, New Jersey. For more information about the Company, please visit . Edetate Calcium Disodium Injection, USP Intravenous or Intramuscular Use Rx Only WARNINGS Edetate calcium disodium injection is capable of producing toxic effects which can be fatal. Lead encephalopathy is relatively rare in adults, but occurs more often in pediatric patients in whom it may be incipient and thus overlooked. The mortality rate in pediatric patients has been high. Patients with lead encephalopathy and cerebral edema may experience a lethal increase in intracranial pressure following intravenous infusion; the intramuscular route is preferred for these patients. In cases where the intravenous route is necessary, avoid rapid infusion. The dosage schedule should be followed and at no time should the recommended daily dose be exceeded. DESCRIPTION Edetate Calcium Disodium injection, USP is a sterile, injectable, chelating agent in concentrated solution for intravenous infusion or intramuscular injection. Each 5 mL single-dose vial contains 1000 mg of edetate calcium disodium (equivalent to 200 mg/mL) in water for injection and sodium hydroxide (as pH adjuster). Chemically, this product is called [[N,N'-1,2-ethanediyl-bis[N-(carboxymethyl)-glycinato]](4-)-N,N’,O,O’,ON,ON’]-, disodium, hydrate, (OC-6-21)-Calciate(2-). CLINICAL PHARMACOLOGY The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron mobilized are not significant. Copper1 is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased.1 Edetate calcium disodium is poorly absorbed from the gastrointestinal tract. In blood, all the drug is found in the plasma. Edetate calcium disodium does not appear to penetrate cells; it is distributed primarily in the extracellular fluid with only about 5% of the plasma concentration found in spinal fluid. The half life of edetate calcium disodium is 20 to 60 minutes. It is excreted primarily by the kidney, with about 50% excreted in one hour and over 95% within 24 hours.2 Almost none of the compound is metabolized. The primary source of lead chelated by edetate calcium disodium is from bone; subsequently, soft-tissue lead is redistributed to bone when chelation is stopped.3,4 There is also some reduction in kidney lead levels following chelation therapy. It has been shown in animals that following a single dose of edetate calcium disodium urinary lead output increases, blood lead concentration decreases, but brain lead is significantly increased due to internal redistribution of lead.5 (See WARNINGS .) These data are in agreement with the recent results of others in experimental animals showing that after a five day course of treatment there is no net reduction in brain lead.6 INDICATIONS AND USAGE Edetate calcium disodium injection is indicated for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. Chelation therapy should not replace effective measures to eliminate or reduce further exposure to lead. CONTRAINDICATIONS Edetate calcium disodium injection should not be given during periods of anuria, nor to patients with active renal disease or hepatitis. WARNINGS See boxed warning . PRECAUTIONS General Precautions Edetate calcium disodium may produce the same renal damage as lead poisoning, such as proteinuria and microscopic hematuria. Treatment-induced nephrotoxicity is dose-dependent and may be reduced by assuring adequate diuresis before therapy begins. Urine flow must be monitored throughout therapy which must be stopped if anuria or severe oliguria develop. The proximal tubule hydropic degeneration usually recovers upon cessation of therapy. Edetate calcium disodium must be used in reduced doses in patients with pre-existing mild renal disease. Patients should be monitored for cardiac rhythm irregularities and other ECG changes during intravenous therapy. Information for patients Patients should be instructed to immediately inform their physician if urine output stops for a period of 12 hours. Laboratory tests Urinalysis and urine sediment, renal and hepatic function and serum electrolyte levels should be checked before each course of therapy and then be monitored daily during therapy in severe cases, and in less serious cases after the second and fifth day of therapy. Therapy must be discontinued at the first sign of renal toxicity. The presence of large renal epithelial cells or increasing number of red blood cells in urinary sediment or greater proteinuria call for immediate stopping of edetate calcium disodium administration. Alkaline phosphatase values are frequently depressed (possibly due to decreased serum zinc levels), but return to normal within 48 hours after cessation of therapy. Elevated erythrocyte protoporphyrin levels (> 35 mcg/dl of whole blood) indicate the need to perform a venous blood lead determination. If the whole blood lead concentration is between 25 to 55 mcg/dl a mobilization test can be considered.7,8 (See Diagnostic Test .) An elevation of urinary coproporphyrin (adults: > 250 mcg/day; pediatric patients under 80 lbs: > 75 mcg/day) and elevation of urinary delta aminolevulinic acid (ALA) (adults: > 4 mg/day; pediatric patients: > 3 mg/m2/day) are associated with blood lead levels > 40 mcg/dl. Urinary coproporphyrin may be falsely negative in terminal patients and in severely iron-depleted pediatric patients who are not regenerating heme.9 In growing pediatric patients long bone x-rays showing lead lines and abdominal x-rays showing radio-opaque material in the abdomen may be of help in estimating the level of exposure to lead. Drug Interactions There is no known drug interference with standard clinical laboratory tests. Steroids enhance the renal toxicity of edetate calcium disodium in animals.7 Edetate calcium disodium interferes with the action of zinc insulin preparations by chelating the zinc.7 Carcinogenesis, Mutagenesis, Impairment of Fertility Long term animal studies have not been conducted with edetate calcium disodium to evaluate its carcinogenic potential, mutagenic potential or its effect on fertility. Pregnancy Category B One reproduction study was performed in rats at doses up to 13 times the human dose and revealed no evidence of impaired fertility or harm to the fetus due to edetate calcium disodium.10 Another reproduction study performed in rats at doses up to about 25 to 40 times the human dose revealed evidence of fetal malformations due to edetate calcium disodium, which were prevented by simultaneous supplementation of dietary zinc.11 There are, however, no adequate and well-controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed. Labor and Delivery Edetate calcium disodium has no recognized use during labor and delivery, and its effects during these processes are unknown. Nursing Mothers It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when edetate calcium disodium is administered to a nursing woman. Pediatric Use Since lead poisoning occurs in pediatric populations and adults but is frequently more severe in pediatric patients, edetate calcium disodium is used in patients of all ages. The intramuscular route is preferred by some for young pediatric patients. In cases where the intravenous route is necessary, avoid rapid infusion. (See WARNINGS .) Urine flow must be monitored throughout therapy; Edetate Calcium Disodium therapy must be stopped if anuria or severe oliguria develops. (See General Precautions .) At no time should the recommended daily dosage be exceeded. (See DOSAGE AND ADMINISTRATION .) ADVERSE REACTIONS The following adverse effects have been associated with the use of edetate calcium disodium: Body as a Whole: pain at intramuscular injection site, fever, chills, malaise, fatigue, myalgia, arthralgia. Cardiovascular: hypotension, cardiac rhythm irregularities. Renal: acute necrosis of proximal tubules (which may result in fatal nephrosis), infrequent changes in distal tubules and glomeruli. Urinary: glycosuria, proteinuria, microscopic hematuria and large epithelial cells in urinary sediment. Nervous System: tremors, headache, numbness, tingling. Gastrointestinal: cheilosis, nausea, vomiting, anorexia, excessive thirst. Hepatic: mild increases in SGOT and SGPT are common, and return to normal within 48 hours after cessation of therapy. Immunogenic: histamine-like reactions (sneezing, nasal congestion, lacrimation), rash. Hematopoietic: transient bone marrow depression, anemia. Metabolic: zinc deficiency, hypercalcemia. To report SUSPECTED ADVERSE REACTIONS, contact Rising Pharma Holdings, Inc. at 1-844-874-7464 or FDA at 1-800-FDA-1088 or . OVERDOSAGE Symptoms Inadvertent administration of 5 times the recommended dose, infused intravenously over a 24 hour period, to an asymptomatic 16 month old patient with a blood lead content of 56 mcg/dl did not cause any ill effects. Edetate calcium disodium can aggravate the symptoms of severe lead poisoning, therefore, most toxic effects (cerebral edema, renal tubular necrosis) appear to be associated with lead poisoning. Because of cerebral edema, a therapeutic dose may be lethal to an adult or a pediatric patient with lead encephalopathy. Higher dosage of edetate calcium disodium may produce a more severe zinc deficiency. Treatment Cerebral edema should be treated with repeated doses of mannitol. Steroids enhance the renal toxicity of edetate calcium disodium in animals and, therefore, are no longer recommended.7 Zinc levels must be monitored. Good urinary output must be maintained because diuresis will enhance drug elimination. It is not known if edetate calcium disodium is dialyzable. DOSAGE AND ADMINISTRATION When a source for the lead intoxication has been identified, the patient should be removed from the source, if possible. The recommended dose of edetate calcium disodium for asymptomatic adults and pediatric patients whose blood lead level is 20 mcg/dl (World Health Organization recommended upper allowable level) is 1000 mg/m2/day whether given intravenously or intramuscularly. (See Surface Area Nomogram.) For adults with lead nephropathy, the following dosing regimen has been suggested: 500 mg/m2 every 24 hours for 5 days for patients with serum creatinine levels of 2 to 3 mg/dl, every 48 hours for 3 doses for patients with creatinine levels of 3 to 4 mg/dl, and once weekly for patients with creatinine levels above 4 mg/dl. These regimens may be repeated at one month intervals.12 Edetate calcium disodium, used alone, may aggravate symptoms in patients with very high blood lead levels. When the blood lead level is > 70 mcg/dl or clinical symptoms consistent with lead poisoning are present, it is recommended that edetate calcium disodium be used in conjunction with BAL (dimercaprol). Please consult published protocols and specialized references for dosage recommendations of combination therapy.14-18 Therapy of lead poisoning in adults and pediatric patients with edetate calcium disodium is continued over a period of five days. Therapy is then interrupted for 2 to 4 days to allow redistribution of the lead and to prevent severe depletion of zinc and other essential metals. Two courses of treatment are usually employed; however, it depends on severity of the lead toxicity and the patient’s tolerance of the drug. Edetate calcium disodium is equally effective whether administered intravenously or intramuscularly. The intramuscular route is used for all patients with overt lead encephalopathy and this route is preferred by some for young pediatric patients. Acutely ill individuals may be dehydrated from vomiting. Since edetate calcium disodium is excreted almost exclusively in the urine, it is very important to establish urine flow with intravenous fluid administration before the first dose of the chelating agent is given; however, excessive fluid must be avoided in patients with encephalopathy. Once urine flow is established, further intravenous fluid is restricted to basal water and electrolyte requirements. Administration of edetate calcium disodium should be stopped whenever there is cessation of urine flow in order to avoid unduly high tissue levels of the drug. Edetate calcium disodium must be used in reduced doses in patients with pre-existing mild renal disease. Intravenous Administration Add the total daily dose of edetate calcium disodium (1000 mg/m2/day) to 250-500 mL of 5% dextrose or 0.9% sodium chloride injection. The total daily dose should be infused over a period of 8 to 12 hours. Discard unused portion. Edetate calcium disodium injection is incompatible with 10% dextrose, 10% invert sugar in 0.9% sodium chloride, lactate Ringer’s, Ringer’s, one-sixth molar sodium lactate injections, and with injectable amphotericin B and hydralazine hydrochloride. Intramuscular Administration The total daily dosage (1000 mg/m2/day) should be divided into equal doses spaced 8 to 12 hours apart. Discard unused portion. Lidocaine or procaine should be added to the edetate calcium disodium injection to minimize pain at the injection site. The final lidocaine or procaine concentration of 5 mg/mL (0.5%) can be obtained as follows: 0.25 mL of 10% lidocaine solution per 5 mL concentrated edetate calcium disodium; 1 mL of 1% lidocaine or procaine solution per mL of concentrated edetate calcium disodium. When used alone, regardless of method of administration, edetate calcium disodium should not be given at doses larger than those recommended. Diagnostic Test Several methods have been described for lead mobilization tests using edetate calcium disodium to assess body stores.7, 9,12,13,18 These procedures have advantages and disadvantages that should be reviewed in current references. Edetate calcium disodium mobilization tests should not be performed in symptomatic patients and in patients with blood lead levels above 55 mcg/dl for whom appropriate therapy is indicated. Parenteral drugs should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. HOW SUPPLIED Edetate Calcium Disodium injection, USP 5 mL single-dose vial (NDC 64980-588-05 ) containing 200 mg of edetate calcium disodium per mL (1000 mg per vial), in boxes containing 5 vials (NDC 64980-588-51 ). Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature]. Rx Only This product is non-returnable. REFERENCES 1. Thomas DJ, Chisolm JJ. Lead, zinc and copper decorporation during calcium disodium ethylene diamine tetraacetate treatment of lead-poisoned children. J Pharmacol Exp Therapeu 1986; 239: 829–835. 2. The Pharmacological Basis of Therapeutics, 7th edition, Goodman and Gilman, editors. MacMillan Publishing Company, New York, 1985, pp. 1619–1622. 3. Hammond PB, Aronson AL, Olson WC. The mechanism of mobilization of lead by ethylenediaminetetraacetate. J Pharmacol Exp Therapeu 1967; 157: 196–206. 4. Van deVyver FL, D’Haese PC, Visser WJ, et al. Bone lead in dialysis patients. Kidney Intl 1988; 33: 601–607. 5. Cory-Slecta DA, Weiss B, Cox C. Mobilization and redistribution of lead over the course of calcium disodium ethylene diamine tetraacetate chelation therapy. J Pharmacol Exp Therapeu 1987; 243: 804–813. 6. Chisolm JJ. Mobilization of lead by calcium disodium edetate. Am J Dis Child 1987;141: 1256–1257. 7. Drug Evaluations, 6th Edition, American Medical Association, Saunders, Philadelphia, 1986, pp. 1637–1639. 8. Centers for Disease Control: Preventing lead poisoning in young children. Atlanta, GA, Department of Health and Human Services, 1985 Jan. 9. Finberg L, Rajagopal V. Diagnosis and treatment of lead poisoning in children. J Family Med 1985 April: 3–12. 10. Schardein JL, Sakowski R, Petrere J, et al. Teratogenesis studies with EDTA and its salts in rats. Toxicol Appl Pharmacol 1981; 61: 423–428. 11. Swenerton H, Hurley LS. Teratogenic effects of a chelating agent and their prevention by zinc. Science 1971; 173: 62–64. 12. American Hospital Formulary Service, Drug Information, 1988, pp. 1695–1698. 13. Markowitz ME, Rosen JF. Assessment of lead stores in children: Validation of an 8-hour CaNa2EDTA (Edetate Calcium Disodium) provocative test. J Pediatrics 1984;104: 337–341. 14. Piomelli S, Rosen JF, Chisolm JJ, et al. Management of childhood lead poisoning. J Pediatrics 1984; 105: 523–532. 15. Sachs HK, Blanksma LA, Murray EF, et al. Ambulatory treatment of lead poisoning: Report of 1,155 cases. Pediatrics 1970; 46: 389. 16. Chisolm JJ. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatrics 1968; 73: 1. 17. Coffin R, Phillips JL, Staples WI, et al. Treatment of lead encephalopathy in children. J Pediatrics 1966; 69: 198–206. 18. Chisolm JJ. Increased lead absorption and acute lead poisoning. Current Pediatric Therapy 12, Gillis and Kagan, editors, WB Saunders, Philadelphia, 1986, pp. 667–671. Distributed by: Rising Pharma Holdings, Inc. East Brunswick, NJ 08816. Made in India Contacts For Media Inquiries: Marina Wissa, (201) 961 9013 mediainquiries@risingpharma.com For Customer Service Inquiries: Jason Eisner, (201) 961 9000 customerservice@risingpharma.com

Clinical ResultDrug Approval

27 Nov 2023

·www.medicaldesignandoutsourcing.com

Researchers develop therapy for metal poisoning from implants

Researchers say they found a way to protect people from heavy metal poisoning as a result of toxicity from cobalt implants. Cobalt was widely used for hip and knee joint replacements due to strength and durability, but this led to cases of heavy metal poisoning. Toxicity can arise from cobalt and other metals if they accumulate in body tissues at high levels. After years of implant wear and tear, metal particles can build up around the joint and cause pain, inflammation and dark discoloration. Teams at the University of Connecticut School of Medicine and Carnegie Mellon say they can protect people from this toxicity, called metallosis. They say implant removal represents “the obvious solution.” However, invasive revision joint surgery brings risk with it. According to the team, traditional chelation therapy is another option. In this therapy, a drug binds the heavy metal and allows the body to excrete it. However, this has a difficult time penetrating joints and surrounding tissues. Researchers found that injecting a material made of traditional chelator combined with a molecule naturally found in the fluid surrounding the joints makes an effective, less invasive therapy to clear out cobalt. They used a chelator called British anti-Lewisite (BAL). This treatment originally helped soldiers poisoned with arsenic-containing Lewisite during World War II. The teams attached the BAL to hyaluronic acid and injected it into the hip joints of rats with cobalt metallosis. Within hours, they say the acid cleared a great deal of cobalt into the bloodstream and kidneys so the rats could excrete it. “This unique approached developed by teams at The Cato T. Laurencin Institute and the department of chemistry at Carnegie Mellon University offer a possible breakthrough treatment for metal ion disease after joint replacement,” said Dr. Cato Laurencin, CEO of the Cato T. Laurencin Institute for Regenerative Engineering. “Now that we know it works in animals, our hope is to eventually bring this type of therapy to humans,” he says.

27 Jul 2023

·endpts.com

Akorn’s bankruptcy, recalls bring a drug to treat lead poisoning into shortage

A drug used to treat lead poisoning is now in short supply after Akorn Pharmaceuticals filed for bankruptcy and many of its products were recalled this spring. Dimercaprol is on the FDA’s drug shortages list , with no date for resolution listed. It’s “very frustrating” not to have an essential antidote available, as another injectable product that can be used to treat lead poisoning is also not readily available, according to Erin Fox, an expert on drug shortages and an adjunct professor at the College of Pharmacy at the University of Utah. Unlock this article instantly, along with access to limited free monthly articles and our suite of newsletters

100 Deals associated with Dimercaprol

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KEGG	Wiki	ATC	Drug Bank
D00167	Dimercaprol	V03AB09	DB06782

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10 top approved records.

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Indication	Country/Location	Organization	Date
Heavy Metal Poisoning	JP	Alfresa Pharma Corp.	01 Jun 1960
Lead Poisoning	US	Provepharm SAS	06 May 1946
Mercury Poisoning	US	Provepharm SAS	06 May 1946

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