Cysteamine

77.15

77.15

200-463-0

5UX2SD1KE2

647528

DTXSID3022875

Crystals by sublimation in vacuo|Crystals from alcohol

A16AA04|S01XA21|A - Alimentary tract and metabolism|S - Sensory organs

29309090

27

-0.4

White to slightly yellow Powder

1.0±0.1 g/cm3

99.5 °C

130 °C

34.6±22.6 °C

1.486

Freely soluble in water.In water, soluble at 20 deg C, value not given

2-8°C

2.45 mm Hg at 25 deg C (est)

Peritoneal-rat LD50: 232 mg/kg; oral-mouse LD50: 625 mg/kg

Flammable; burning produces toxic nitrogen oxides and sulfur oxide fumes

Disagreeable odor

10.4None

Henry's Law constant = 3.6X10-7 atm-cu m/mol at 25 °C (est)

10.4|pKa1 = 8.19 (thiol); pKa2 = 10.75 (amine) (c= 0.01 moles/L, mixed constants)

Oxidizes to cystamine on standing in air|Hydroxyl radical reaction rate constant = 7.3X10-11 cu cm/molec-sec at 25 °C (est)|Crystals from alcohol, mp 70.2 to 70.7 °C. Soluble in water, alcohol. /Hydrochloride/

3259

3

22-36/37/38

26-36

KJ0175000

Xn

Warehouse ventilated, low temperature and dry

Stable, but may be air-sensitive. Incompatible with strong oxidizing agents.

P261-P305 + P351 + P338

H302-H315-H319-H335

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl cysteamine bitartrate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Cysteamine Bitartrate/

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 41 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Danger|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P264, P270, P281, P301+P312, P308+P313, P330, P405, and P501

moderately toxic

Two cases of human overdoses with cysteamine are recorded in the literature, according to prescribing information. In one case, vomiting was immediate after the administration of cysteamine, and the patient did not experience other symptoms. A 200 to 250 mg/kg dose was accidentally ingested by a healthy 13-month-old child. Vomiting and dehydration followed. A full recovery was made after hospitalization and the replenishment of fluids. There is no known antidote for an overdose with cysteamine. In the case of an overdose, provide supportive treatment, especially to the cardiovascular and respiratory systems. Hemodialysis may be useful in some cases due to the fact that cysteamine has poor plasma protein binding.

During long term use of cysteamine in preregistration studies, serum ALT elevations occurred in a small proportion of treated subjects, but the background rate of serum enzyme elevations in this population is high and was not defined in the open label studies. There have been reports of more marked enzyme elevations during high dose therapy with cysteamine, with recurrence on reexposure. These abnormalities were invariably asymptomatic and rapidly reversed with dose adjustment. In addition, patients with cystinosis appear to be at risk for developing nodular regenerative hyperplasia and noncirrhotic portal hypertension. The role of long term cysteamine therapy in these hepatic complications is not clear. There have been no reports of clinically apparent, acute liver injury with jaundice attributable to cysteamine, although it has had only limited wide scale use.

LD50 Mouse oral 625 mg/kg|LD50 Mouse ip 250 mg/kg

Cysteamine is 52% plasma protein bound, and is mostly bound to albumin.

Cysteamine's production and use as an antidote to acetaminophen, experimentally as a radioprotective agent, and as a research chemical in the study of duodenal ulcers(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 33(SRC), determined from a structure estimation method(2), indicates that cysteamine is expected to have very high mobility in soil(SRC). Volatilization of cysteamine from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.6X10-7 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Cysteamine is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.4 mm Hg(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2005).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 33(SRC), determined from a structure estimation method(2), indicates that cysteamine is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 3.6X10-7 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). The pKa1 and pKa2 values for cysteamine are 8.19 and 10.75(5), respectively, indicating that this compound will primarily exist in the cation form in the environment and cations generally adsorb more strongly to organic carbon and clay than their neutral counterparts(6). According to a classification scheme(7), an estimated BCF of 3(SRC), from an estimated log Kow of -0.20(8) and a regression-derived equation(9), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2005).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), cysteamine, which has an estimated vapor pressure of 2.45 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase cysteamine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 5 hours(SRC), calculated from its rate constant of 7.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Cysteamine does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of cysteamine with photochemically-produced hydroxyl radicals has been estimated as 7.3X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Cysteamine is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2). Cysteamine does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated for cysteamine(SRC), using an estimated log Kow of -0.20(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of cysteamine can be estimated to be 33(SRC). According to a classification scheme(2), this estimated Koc value suggests that cysteamine is expected to have very high mobility in soil. The pKa1 and pKa2 values for cysteamine are 8.19 and 10.75(3), respectively, indicating that this compound will primarily exist in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

The Henry's Law constant for cysteamine is estimated as 3.6X10-7 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that cysteamine is expected to be essentially nonvolatile from water surfaces(2). Cysteamine is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.45 mm Hg(SRC), determined from a fragment constant method(3).

Occupational exposure to cysteamine may occur through inhalation and dermal contact with this compound at workplaces where cysteamine is produced or used. Exposure to cysteamine among the general population may be limited to those administered the drug cysteamine bitartrate. (SRC)

The bitartrate salt of cysteamine is used for the oral treatment of nephropathic cystinosis and cystinuria in children 6 years old and above, and adults. The hydrochloride salt, used in eye drop preparations, is indicated for the treatment of corneal cystine crystal accumulation in patients with cystinosis.|FDA Label|Procysbi is indicated for the treatment of proven nephropathic cystinosis. Cysteamine reduces cystine accumulation in some cells (e.g. leukocytes, muscle and liver cells) of nephropathic cystinosis patients and, when treatment is started early, it delays the development of renal failure.|Cystadrops is indicated for the treatment of corneal cystine crystal deposits in adults and children from 2 years of age with cystinosis.|Cystagon is indicated for the treatment of proven nephropathic cystinosis. Cysteamine reduces cystine accumulation in some cells (e.g. leukocytes, muscle and liver cells) of nephropathic cystinosis patients and, when treatment is started early, it delays the development of renal failure.|Treatment of corneal cystine deposits,

Cysteamine is a simple aminothiol molecule that is used to treat nephropathic cystinosis, due to its ability to decrease the markedly elevated and toxic levels of intracellular cystine that occur in this disease and cause its major complications. Cysteamine has been associated with serum enzyme elevations when given intravenously in high doses, but it has not been shown to cause clinically apparent acute liver injury.

Genetic Disorder Agents

Cysteamine is indicated for the management of nephropathic cystinosis in children and adults. /Included in US product labeling/|Nephropathic cystinosis is a rare, autosomal recessive lysosomal storage disorder caused by mutations in the CTNS gene that codes for a cystine transporter in the lysosomal membrane. Affected patients store 50-100 times the normal amounts of cystine in their cells, and suffer renal tubular and glomerular disease, growth retardation, photophobia, and other systemic complications, including a myopathy and swallowing dysfunction. Using videofluoroscopy and ultrasound examinations, we assessed the swallowing function of 101 patients with nephropathic cystinosis on their most recent admission to the National Institutes of Health Clinical Center between 1987 and 2004. These patients ranged in age from 6 to 45 years; more than half had significant complaints of swallowing difficulty. On examination of barium swallow, the oral, pharyngeal, and esophageal phases of swallowing were abnormal in 24%, 51%, and 73% of patients, respectively. The frequency of dysfunction increased with age for each phase of swallowing. Both the Swallowing Severity Score (a measure of dysfunction on barium swallow) and the Oral Muscle Composite Score (a reflection of vocal strength, oral-facial movement, and tongue and lip function) increased (that is, worsened) with the number of years that a patient was not receiving treatment with cysteamine, the cystine-depleting agent of choice in cystinosis. The severity scores decreased with the number of years on cysteamine therapy. The Swallowing Severity Score varied directly with the severity of muscle disease, but was not correlated with the presence or absence of the 57-kb CTNS deletion that commonly occurs in nephropathic cystinosis patients. We conclude that swallowing dysfunction in cystinosis presents a risk of fatal aspiration, correlates with the presence of muscle atrophy, and, based on cross-sectional data, increases in frequency with age and number of years without cysteamine treatment. Cystine-depleting therapy with cysteamine should be considered the treatment of choice for both pre- and posttransplant cystinosis patients.|/EXPL THER/ N-Acetylcysteine (NAC) is protective against acetaminophen-induced hepatotoxicity primarily by providing precursor for the glutathione synthetase pathway, while cysteamine has been demonstrated to alter the cytochrome P-450 dependent formation of toxic acetaminophen metabolite. Mice administered acetaminophen (500 mg/kg) had elevations of serum alanine aminotransferase (ALT) to 273.0 +/- 37.5 and 555.8 +/- 193.4 U/mL at 12 and 24 h, respectively, after injection. Administration of cysteamine (100 mg/kg) or NAC (500 mg/kg) significantly reduced serum ALT activity (p less than 0.001). Reducing the dose of NAC or cysteamine by 50% greatly reduced their hepatoprotective effect while the co-administration of the reduced doses of NAC (250 mg/kg) and cysteamine (50 mg/kg) following acetaminophen overdose prevented elevation of serum ALT activity (39.2 +/- 1.17 and 32.5 +/- 5.63 U/mL at 12 and 24 h post-injection, p less than 0.001) and preserved normal mouse hepatic histology. Neither NAC (500 mg/kg), cysteamine (100 mg/kg), or the lower doses in combination of both agents were found to alter the half-life or peak levels of acetaminophen. Liver microsomal aryl hydrocarbon hydroxylase activity measured 24 h after drug administration was not significantly different between treatment groups and controls receiving only saline. These results indicate a possible role for the concomitant use of NAC and cysteamine in the prevention of hepatic necrosis following toxic doses of acetaminophen. Neither decrease in plasma acetaminophen levels nor depression of cytochrome P-450 enzyme activity appears to be the mechanism of protection when these doses of NAC, cysteamine, or both drugs together are administered with a toxic dose of acetaminophen in mice.|Although renal disease is the most prominent feature of the lysosomal storage disease cystinosis, corneal cystine crystal formation remains a major complication, leading to photophobia, corneal erosions, and keratopathies. Moreover, the extent of corneal crystal accumulation reflects the course and severity of the disease itself, and the cornea is accessible to direct examination. Therefore, we employed a scoring system, based on a library of slit-lamp photographs of corneas with increasing crystal densities (0.00-3.00), to assess the degree of crystal accumulation in 170 patients with nephropathic cystinosis examined at the National Institutes of Health between 1976 and 2000. None of the patients had received topical cystine-depleting therapy at the time of the evaluation. In this natural history study, infants in the first year of life had absent or minimal corneal crystals, i.e., a corneal cystine crystal score (CCCS) of 0 or 0.25. However, the CCCS increased linearly with age, such that every patient had visible crystals by 16 months of age, and plateaued at approximately 3.00 by early adolescence. Longitudinal studies in representative patients support the cross-sectional results. Individuals homozygous for the common 57-kb deletion involving the cystinosis gene (CTNS) displayed the same course of corneal crystal accumulation as did individuals not bearing the large deletion. Patients with ocular or nonnephropathic cystinosis had CCCSs that were, in general, half those expected for patients with nephropathic cystinosis of the same age. Administration of 0.55% cysteamine eyedrops, given 6 to 12 times per day, dissolved corneal cystine crystals in 10 representative patients with nephropathic cystinosis aged 1 to 32 years within 8 to 41 months.|The necessity to apply near-toxic amounts of radioprotective drugs to achieve adequate protection during radiation treatments represents a major problem in human medicine. One of the promising strategies to suppress the toxicity of these drugs involves their incorporation into biocompatible polymers. In this study cysteamine (Cy) was attached to poly(oxyethylene phosphate), POEP, via an ionic bond. Radioprotection of E. coli B cells by this substance and its acute toxicity on male C57 BL mice were measured. The toxicity of Cy immobilized within the poly(oxyethylene phosphate) was significantly lower in comparison to pure Cy while its radioprotective efficiency remained high at half the maximum tolerable dose. The high radioprotective efficiency of the Cy/POEP complexes was further confirmed on mice at different polymer molecular weight characteristics, drug immobilization degrees, application times, and doses. It was found that POEP with molecular weight 4700 Da and containing 24% repeating units with attached Cy has the highest protection potential combined with a depot effect.

The most frequent adverse reactions seen involve the GI and central nervous systems. These are especially prominent at the initiation of therapy. Temporarily suspending treatment, then gradual reintroduction may be effective in improving tolerance. The most common events (> 5%) were vomiting (35%), anorexia (31%), fever (22%), diarrhea (16%), lethargy 11%) and rash (7%). Other adverse reactions are as follows: CNS: Somnolence; encephalopathy; headache; seizures; ataxia; confusion; tremor; hyperkinesia; decreased hearing; dizziness; jitteriness. GI: Nausea; bad breath; abdominal pain; dyspepsia; constipation; gastroenteritis; duodenitis; duodenal ulceration. Psychiatric: Nervousness; abnormal thinking; depression; emotional lability; hallucinations; nightmares. Miscellaneous: Abnormal liver function; anemia; leukopenia; dehydration; hypertension; urticaria.|Cysteamine has occasionally been associated with reversible leukopenia and abnormal liver function studies. Therefore, monitor blood counts and liver function studies.|Patients sensitive to penicillamine may be sensitive to this medication also.|FDA Pregnancy category C: Adequate, well controlled human studies are lacking, and animal studies have shown risk to the fetus or are lacking as well. There is a chance of fetal harm if the drug is given during pregnancy; but the potential benefits may outweigh the potential risk.|For more Drug Warnings (Complete) data for CYSTEAMINE (11 total), please visit the HSDB record page.

Cystine accumulation is the cause of organ damage in cystinosis. Cysteamine prevents the accumulation of cystine crystals in the body and is specifically prescribed to prevent kidney and eye damage. Cysteamine converts cystine into a form that may easily exit cells, preventing harmful accumulation.

Compounds and drugs that react with CYSTINE and convert it into a compound that can be more easily metabolized or intracellularly transported. Drugs in this class have been used to treat CYSTINOSIS. (See all compounds classified as Cystine Depleting Agents.)

Orally administered cysteamine is absorbed in the gastrointestinal tract and reaches its maximum plasma concentration in about 1.4 hours, with some variation according to the type of formulation (delayed versus immediate-release). One pharmacokinetic study of adults with Cystic Fibrosis revealed a Cmax of 2.86 mg/L.The maximum plasma concentration after administration of cysteamine eye drops is unknown, however, it is likely to be considerably lower than oral administration. According to prescribing information, the AUC 0-12 h for the delayed-release oral tablets is 99.26 ± 44.2 μmol*h/L with a Cmax of 27.70 ± 14.99 μmol/L. The AUC 0-12 for the immediate-release tablets is 192.00 ± 75.62 μmol*h/L with a Cmax of 37.72 ± 12.10 μmol/L.|Cysteamine has a volume of distribution of about 129 L, according to one pharmacokinetic study. Prescribing information indicates a volume of distribution of 382 L for the delayed-release formulation and 198 L for the immediate-release preparation. It is known to cross the blood-brain barrier.|The plasma clearance of cysteamine is about 1.2 - 1.4 L/min. One reference mentions a clearance of 89.9 L/h in patients with Cystic Fibrosis.|/Cysteamine is/ poorly bound to plasma proteins.|It is not known whether cysteamine is distributed into breast milk.|In a patient with cystinosis, an oral dose of cysteamine was absorbed rapidly, with plasma cysteamine reaching a maximum of 56 microM 1 h after the dose. By 1.8 h the plasma cysteamine concentration had decreased to one-half the maximum value.|Cysteamine bitartrate was administered to 11 cystinosis patients at their regular dose level in a single-dose, open-label, steady-state study. Blood samples were collected and analysed for plasma cysteamine and white blood cell cystine content and pharmacokinetic and pharmacodynamic parameters estimated by NONMEM analysis using a linked pharmacokinetic-pharmacodynamic model. Cysteamine was rapidly cleared from the plasma (mean CL/F = 32.3 mL min(-1) kg(-1), range = 17.3-52.2), appeared to be extensively distributed (mean Vss/F = 15.1 l, range 2.7-32.3) and exhibited a mean Tmax of 1.4 hr. White blood cell cystine content post-dosing was significantly decreased compared with pre- and post-dose values (average decrement approximately 47%). A counter-clockwise hysteresis was noted in all patients, suggestive of a lag time (mean Tlag = 0.44 hr, range 0.22-0.92) between drug concentration and effect. The results of this study establish that cysteamine is rapidly cleared from the plasma but that an every 6 hr dosing interval adequately maintains white blood cell cystine content below the target of 1 nmol cystine per mg protein. /Cysteamine bitartrate/|Cysteamine (beta-mercaptoethylamine, MEA) is currently used to treat children with nephropathic cystinosis. In this study MEA was compared to phosphocysteamine (MEAP), a phosphorothioester that tastes and smells better than MEA, with respect to its ability to elevate plasma MEA and deplete leukocytes of cystine. Studies were performed in six children with nephropathic cystinosis ranging in age from 2 to 10 yr. After equimolar oral doses of either MEA or MEAP plasma cysteamine was determined at various times for 6 h. MEA was determined by sodium borohydride reduction followed by high-performance liquid chromatography separation and electrochemical detection. Leukocyte cystine was measured before and 1 and 6 h after drug administration. Peak plasma MEA was obtained 30 min to 1 hr after a dose and was not significantly different when MEA (48.6 +/- 10.7, mean +/- SD) or MEAP (54.1 +/- 20.2) was given. Significant plasma MEA concentrations were seen as early as 15 min after an oral dose, indicating rapid absorption. Analysis of vomitus indicated that hydrolysis of the phosphate group of MEAP occurs in the stomach. The percent decrease in leukocyte cystine content obtained with MEA administration (61.9%) was not significantly different from the decrease observed when MEAP was administered (65.3%). MEA and MEAP appear to be equally effective in their cystine-depleting properties.

There is limited information in the literature regarding the metabolism of cysteamine. This drug undergoes significant first-pass metabolism.

The half-life of cysteamine is about 3.7 hours.

Individuals born without the ability to metabolize cystine suffer from cystinosis, a rare genetic disorder characterized by the widespread accumulation of cystine crystals throughout the body and eye tissues. The cystine crystals may cause considerable damage, particularly in the renal tissues and corneal tissues. In some cases, renal failure can occur during childhood if the condition is left untreated. Other organs that may be affected by cystinosis include the CNS, thyroid, pancreas, muscle tissues, and gonads. Cysteamine converts cystine to cysteine and cysteine-cysteamine mixed disulfides, reducing the buildup of corneal cystine crystals. This drug participates in a thiol-disulfide interchange reaction with lysosomes, leading to cysteine exit from the lysosome in patients diagnosed with cystinosis.|Cysteamine is an aminothiol that converts cystine to cysteine and cysteine-cysteamine mixed disulfide, both of which can pass through the lysosomal membrane of patients with cystinosis. In the nephropathic form of cystinosis, the accumulation of cystine and the formation of crystals damage various organs, especially the kidney. Cysteamine improves glomerular function without affecting tubular function.

Should overdose occur, appropriately support the respiratory and cardiovascular systems. No specific antidote is known. ... Hemodialysis may be considered since cysteamine is poorly bound to plasma proteins.|Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poison A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poison A and B/

/SIGNS AND SYMPTOMS/ The most frequent adverse reactions seen involve the GI and central nervous systems. These are especially prominent at the initiation of therapy. Temporarily suspending treatment, then gradual reintroduction may be effective in improving tolerance. The most common events (> 5%) were vomiting (35%), anorexia (31%), fever (22%), diarrhea (16%), lethargy 11%) and rash (7%). Other adverse reactions are as follows: CNS: Somnolence; encephalopathy; headache; seizures; ataxia; confusion; tremor; hyperkinesia; decreased hearing; dizziness; jitteriness. GI: Nausea; bad breath; abdominal pain; dyspepsia; constipation; gastroenteritis; duodenitis; duodenal ulceration. Psychiatric: Nervousness; abnormal thinking; depression; emotional lability; hallucinations; nightmares. Miscellaneous: Abnormal liver function; anemia; leukopenia; dehydration; hypertension; urticaria.

2 Aminoethanethiol

U.S.- 50 mg (Rx) Cystagon. 150 mg (Rx) Cystagon.

While data specific to cysteamine were not available(SRC, 2005), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2). Studies have indicated that several polar pharmaceutically active compounds can leach through subsoils into aquifers(1).

Human drugs -> Orphan -> Procysbi -> EMA Drug Category|Other alimentary tract and metabolism products -> Human pharmacotherapeutic group|Human drugs -> Orphan -> Cystadrops -> EMA Drug Category|Ophthalmologicals -> Human pharmacotherapeutic group|Human drugs -> Cystagon -> EMA Drug Category|Human drugs -> Orphan -> Dropcys -> EMA Drug Category|Human drugs -> Rare disease (orphan)|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients