excretion

MDCG sodium (N-methyl-N-dithiocarboxyglucamine sodium) is a metal chelator that promotes biliary excretion of Cd.

DL-Penicillamine (3-Sulfanylvaline) is a chelating agent recommended for the removal of excess copper in patients with Wilson's disease. DL-Penicillamine is only found in individuals that have used or taken this drug. It is the most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease. From in vitro studies which indicate that one atom of copper combines with two molecules of DL-penicillamine. DL-Penicillamine also reduces excess cystine excretion in cystinuria. This is done, at least in part, by disulfide interchange between DL-penicillamine and cystine, resulting in the formation of penicillamine-cysteine disulfide, a substance that is much more soluble than cysteine and is excreted readily. DL-Penicillamine interferes with the formation of cross-links between tropocollagen molecules and cleaves them when newly formed. The mechanism of action of DL-penicillamine in rheumatoid arthritis is unknown although it appears to suppress disease activity. Unlike cytotoxic immunosuppressants, DL-penicillamine markedly lowers IgM rheumatoid factor but produces no significant depression in absolute levels of serum immunoglobulins. Also unlike cytotoxic immunosuppressants which act on both, DL-penicillamine in vitro depresses T-cell activity but not B-cell activity.

Dapagliflozin (BMS-512148) is a selective sodium-glucose co-transporter subtype 2 (SGLT2) inhibitor with antihyperglycemic activity.

Trans-2-butene-1,4-dicarboxylic acid (3-Hexenedioic Acid) is a normal human unsaturated dicarboxylic acid metabolite with increased excretion in patients with Dicarboxylic aciduria caused by fatty acid metabolism disorders The urinary excretion of Trans-2-butene-1,4-dicarboxylic acid is increased in conditions of augmented mobilization of fatty acids or inhibited fatty acid oxidation.

NSC-16590 (2-Aminoisobutyric acid) is a nonprotein amino acid (is an end product of pyrimidine Metabolism) excreted in the urine of about 5% of healthy individuals, and high excretion is an autosomal recessive phenotype.

Cholic Acid (Cholate) is a major primary bile acid produced in the liver and usually conjugated with glycine or taurine. Cholic acid facilitates fat absorption and cholesterol excretion.

Diphenmanil methylsulfate (Diphemanil mesylate), a quaternary ammonium anticholinergic, binds muscarinic acetylcholine receptors and thus decreases secretory excretion of stomach acids, sweat, and saliva.

EDTA, Disodium Salt, Dihydrate (Ethylenediaminetetraacetic acid disodium dihydrate) is a metal ion chelator used as a protease inhibitor.EDTA, Disodium Salt, Dihydrate is a molecule that is ineffective against cellulase activity and is widely used in protein purification.EDTA, Disodium Salt, Dihydrate promotes the excretion of cellulase by binding to the metals and promotes their excretion.

Potassium oxonate (Potassium azaorotate) is a uricase inhibitor that prevents metabolism and excretion of uric acid and induces embryotoxicity and nephrotoxicity in rats.

Pyrrole-2-carboxylic acid (Minaline) was first identified as a degradation product of sialic acids, then as a derivative of the oxidation of the D-hydroxyproline isomers by mammalian D-amino acid oxidase. The latter relationship results from the lability of the direct oxidation product, A'-pyrroline-4-hydroxy-2-carboxylic acid, which loses water spontaneously to form the pyrrole. A similar reaction is catalyzed by the more specific allohydroxy-D-proline oxidase of Pseudomonas. In whole animal observations, pyrrole-2-carboxylate (PCA) ' was identified in rat or human urine after administration of the D-isomers of hydroxyproline, a finding ascribable to the action of D-amino acid oxidase. Urinary excretion of N-(pyrrole-2-carboxyl) glycine has been reported in a 5-year-old affected with type II hyperprolinemia; The child has mild developmental delay, recurrent seizures of the grand mal type and EEG alterations.

L-Ornithine hydrochloride ((S)-2,5-Diaminopentanoic acid) has an antifatigue effect by increasing the efficiency of energy consumption and promoting the excretion of ammonia. It is one of the key reactants in the urea cycle.

3-Hydroxyisovaleric acid (Beta-Hydroxyisovaleric acid) is an endogenous metabolite excreted in the urine and can serve as an early and sensitive indicator of biotin deficiency.

Cholic acid sodium (SodiumCholate) exhibits a strong spermicidal and antiviral [anti-human immunodeficiency virus (HIV)-1] activity.

Hydrocortisone (Cortisol) is a glucocorticoid hormone secreted by the adrenocortex. Hydrocortisone agonizes the glucocorticoid receptor, which promotes proteolytic metabolism, gluconeogenesis, capillary wall stabilization, and renal calcium excretion, as well as suppressing immune and inflammatory responses.

L-Ornithine ((S)-2,5-Diaminopentanoic acid) exhibits an anti-fatigue function by promoting ammonia excretion and enhancing energy consumption efficiency.

Penicillamine (Artamine), possessing antineoplastic properties, induces apoptosis by a p53-mediated mechanism and inhibits angiogenesis by chelating with copper, a cofactor for angiogenesis. Artamine is a beta dimethyl analog of the amino acid cysteine. As a degradation product of penicillin antibiotics, Artamine chelates with heavy metals and increases their urinary excretion.

Xanthine amine congener trihydrochloride is a potent adenosine antagonist that reverses the reduction in urine flow, sodium excretion and heart rate produced by the adenosine agonist, N6-cyclohexyladenosine.

Norathiol (N-methyl-N-dithiocarboxyglucamine) is an antidote for cadmium poisoning and a metal chelator that promotes the excretion of 109Cd and can be used in the treatment of cadmium poisoning.

Cyclopenthiazide (Cyclomethiazide) is a thiazide diuretic used to treat hypertension and heart failure. It decreases the excretion of calcium ions and uric acid and increases the excretion of sodium and potassium ions.

N-Isovaleroylglycine (Isovaleroylglycine) is an acyl glycine. Acyl glycines are normally minor metabolites of fatty acids. However, the excretion of certain acyl glycines is increased in several inborn errors of metabolism. In certain cases, the measurement of these metabolites in body fluids can be used to diagnose disorders associated with mitochondrial fatty acid beta-oxidation. Acyl glycines are produced through the action of glycine N-acyltransferase which is an enzyme that catalyzes the chemical reaction: acyl-CoA + glycine < -- > CoA + N-acylglycine. N-Isovaleroylglycine is a byproduct of the catabolism of the amino acid leucine. Accumulation of N-Isovaleroylglycine occurs in Isovaleric Acidemia (IVA).

Nitisinone-13C6is intended for use as an internal standard for the quantification of nitisinone by GC- or LC-MS. Nitisinone is an inhibitor of 4-hydroxyphenylpyruvate dioxygenase (HPPD), which converts 4-hydroxyphenylpyruvate (HPPA) to homogentisate in the tyrosine catabolic pathway.1Nitisinone increases urinary levels of HPPA and 4-hydroxyphenyllactate (HPLA) in rats when administered at a dose of 10 mg/kg. Nitisinone (3 mg/kg) prevents the neonatal lethality of fumarylacetoacetate hydrolase (FAH) deficiency in mice when administered to pregnant dams.2It exhibits hepatoprotective effects inFAH-/-mice, such as prevention of increases in plasma levels of aspartate serine aminotransferase (AST) and conjugated bilirubin, when administration is continued following birth at a dose of 1 mg/kg. Nitisinone (100 μg) decreases urinary excretion of homogentisate and increases urinary excretion of HPPA, HPLA, and 4-hydroxyphenylacetate in a mouse model of alkaptonuria induced by ethylnitrosourea.3Formulations containing nitisinone have been used in the treatment of hereditary tyrosinemia type 1 (HT-1). 1.Ellis, M.K., Whitfield, A.C., Gowans, L.A., et al.Inhibition of 4-hydroxyphenylpyruvate dioxygenase by 2-(2-nitro-4-trifluoromethylbenzoyl)-cyclohexane-1,3-dione and 2-(2-chloro-4-methanesulfonylbenzoyl)-cyclohexane-1,3-dioneToxicol. Appl. Pharmacol.133(1)12-19(1995) 2.Grompe, M., Lindstedt, S., al-Dhalimy, M., et al.Pharmacological correction of neonatal lethal hepatic dysfunction in a murine model of hereditary tyrosinaemia type INat. Genet.10(4)453-460(1995) 3.Suzuki, Y., Oda, K., Yoshikawa, Y., et al.A novel therapeutic trial of homogentisic aciduria in a murine model of alkaptonuriaJ. Hum. Genet.44(2)79-84(1999)

(±)8,9-DiHETE is a major metabolite of the 20:5 ω-3 fatty acid eicosapentaenoic acid .[1] It is produced in rat liver microsomes, but not renal microsomes, by the generation of the unstable intermediate 8,9-epoxy eicosatetraenoic acid from EPA by cytochrome P450 monooxygenases. Dietary EPA supplementation in humans results in substantial urinary excretion of vicinal diols, including 8,9, 11,12, and 14,15 forms.[2]

Tetrahydro-11-deoxy cortisol (THS) is the primary urinary metabolite of 11-deoxycortisol. Urinary excretion of THS is elevated in patients with 11β-hydroxylase deficiency, a condition resulting from mutations in the cytochrome P450 (CYP) isoform CYP11B1. Urinary levels of THS are also elevated in patients with adrenocortical carcinoma (ACC) and adrenocortical adenoma (ACA) but are higher in patients with ACC compared to ACA.

AY 31906 is a high ceiling diuretic with a relative potassium-sparing effect. AY 31906 has been shown to produce significant increases in the fractional excretion of sodium and chloride in dogs at a dose that produces no statistically significant changes

CGP-28014 is an inhibitor of catechol-O-methyltransferase. CGP-28014 increases the renal excretion of both dopamine and dihydroxyphenylacetic acid (DOPAC) but does not affect renal sodium handling indicating a different mechanism of action. CGP-28014 sign

Lumasiran sodium, an investigational RNA interference (RNAi) therapeutic agent, targets glycolate oxidase to reduce hepatic oxalate production and urinary oxalate excretion, showing promise in addressing the underlying cause of progressive kidney failure in individuals with primary hyperoxaluria type 1 (PH1).

Advanced glycation end products (AGEs) are compounds formed by non-enzymatic chemical reactions following the bonding of sugars to proteins or lipids during diabetes, uremia, aging, rheumatic arthritis, and other conditions. A receptor for the AGEs (RAGE) binds certain members of this class to initiate cell signaling.[1][2] Pentosidine is a well-characterized natural AGE that is often used as a biomarker for the production of all AGEs. While pentosidine can be measured in urine, the majority of this AGE is catabolized before excretion.[3] Reference：[1]. Neeper, M., Schmidt, A.M., Brett, J., et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. The Journal of Biological Chemisty 267(21), 14998-15004 (1992).[2]. Brett, J., Schmidt, A.M., Yan, S.D., et al. Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. American Journal of Pathology 143(6), 1699-1712 (1993).[3]. Miyata, T., Ueda, Y., Horie, K., et al. Renal catabolism of advanced glycation end products: The fate of pentosidine. Kidney International 53, 416-422 (1998).

Hydrocortisone-d4 is a deuterated compound of Hydrocortisone. Hydrocortisone has a CAS number of 50-23-7. Hydrocortisone, a glucocorticoid receptor agonist, promotes protein catabolism, gluconeogenesis, capillary wall stability, renal excretion of calcium, and suppresses immune and inflammatory responses. Therapeutic Hydrocortisone is a synthetic or semisynthetic analog of natural hydrocortisone hormone produced by the adrenal glands with primary glucocorticoid and minor mineralocorticoid effects.

Advanced glycation end products (AGEs) are compounds that are produced through non-enzymatic chemical reactions when sugars bond with proteins or lipids, occurring in conditions such as diabetes, uremia, aging, and rheumatic arthritis. A specific receptor, known as RAGE, interacts with select AGEs to trigger cell signaling. Pentosidine, a prominently studied natural AGE, serves as a common biomarker for assessing AGE production. Although pentosidine levels can be determined through urine analysis, it is predominantly broken down prior to excretion.

Compound BDEO (URAT1&XO inhibitor 2) serves as a dual-action inhibitor targeting both xanthine oxidase (XO) and URAT1, demonstrating an IC50 value of 3.3 μM for XO inhibition. It effectively impedes uric acid uptake in HEK293 cells with URAT1 expression, evidenced by a Ki of 0.145 μM. In hyperuricemic mice models, the compound has been shown to reduce serum urate levels and uric acid excretion, indicating potential utility for hyperuricemia research [1].

Pregnanetriol is a metabolite of 17α-hydroxyprogesterone .1,2It is formed from 17α-hydroxyprogesterone by reduction of the C-20 ketone.2Urinary levels of pregnanetriol are elevated in patients with 21-hydroxylase deficiency and congenital adrenal hyperplasia.3,4 1.Kamrath, C., Hartmann, M.F., Boettcher, C., et al.Diagnosis of 21-hydroxylase deficiency by urinary metabolite ratios using gas chromatography-mass spectrometry analysis: Reference values for neonates and infantsJ. Steroid Biochem. Mol. Biol.15610-16(2016) 2.Schiffer, L., Barnard, L., Baranowski, E.S., et al.Human steroid biosynthesis, metabolism and excretion are differentially reflected by serum and urine steroid metabolomes: A comprehensive reviewJ. Steroid Biochem. Mol. Biol.194105439(2019) 3.Disorders of steroidogenesis guide to steroid profiling and biochemical diagnosis1(2019) 4.Shackleton, C.H.L.Role of a disordered steroid metabolome in the elucidation of sterol and steroid biosynthesisLipids47(1)1-12(2012)

Hexanoyl glycine is an acylated amino acid that is used as a urinary biomarker for several indications. It is normally biosynthesized from hexanoyl-CoA and glycine by the mitochondrial enzyme glycine N-acyltransferase. Increased urinary excretion of hexanoyl glycine in humans is indicative of a deficiency in medium-chain acyl-CoA dehydrogenase. Increased urinary hexanoyl glycine can also be used as a biomarker for exposure to gamma radiation. Levels of hexanyl glycine can also be elevated during cancer, while they are decreased 20-fold in mice following treatment with the PPARα ligand Wy 14643.

CP21 is an iron chelator that binds to iron in a 3:1 (ligand:iron) ratio. It is active against P. falciparum when used at concentrations of 10 and 100 µM. CP21 inhibits production of prostaglandin I2 induced by epinephrine, arachidonic acid, or A23187 in isolated rat aortic rings with IC50 values of 1.3, 1.3, and 1.4 mM, respectively. It inhibits glutamate-induced oxytosis, as well as decreases iodoacetic acid-induced cytotoxicity in an in vitro model of ischemia, in HT22 mouse hippocampal cells (EC50s = 13 and 9.5 µM, respectively). CP21 (200 mg/kg) increases the excretion of iron, but not copper, zinc, calcium, or magnesium, in rabbits.

L-Glyceric acid sodium, a urinary metabolite, is predominantly found in individuals with the rare inherited metabolic disorder L-glyceric aciduria. This compound is a diagnostic tool for identifying primary hyperoxaluria type 2 (PH2) and distinguishing it from primary hyperoxaluria type 1 (PH1) based on its excretion pattern.

RPR132595A (NPC) hydrochloride, an active metabolite of CPT-11, is produced via cytochrome P-450 3A4 (CYP3A4) metabolism and is ultimately eliminated via urinary excretion [1].

Glucagon significantly impacts protein and amino acid metabolism. It hinders the integration of amino acids into the proteins of the liver, muscle, and pancreas, augmenting nitrogen excretion and stimulating hepatic urea synthesis. Additionally, it elevates hepatic transaminase and urea cycle enzyme levels. Glucagon also enhances hepatic amino acid uptake, facilitating their conversion into liver glycogen, and reduces blood amino acid concentrations [1].

Estrone-3-Glucuronide is a metabolite of the primary premenopausal estrogen 17β-estradiol .1,2Urinary levels of estrone-3-Glucuronide peak approximately 36 hours prior to ovulation and have been used as a marker of fertility in women. 1.Blackwell, L.F., Brown, J.B., and Cooke, D.Definition of the potentially fertile period from urinary steroid excretion rates. Part II. A threshold value for pregnanediol glucuronide as a marker for the end of the potentially fertile period in the human menstrual cycleSteroids63(1)5-13(1998) 2.Adlercreutz, H., Brown, J., Collins, W., et al.The measurement of urinary steroid glucuronides as indices of the fertile period in womenJ. Steroid Biochem.17(6)695-702(1982)

5-chloro Hydrochlorothiazide is a derivative of hydrochlorothiazide, which is a diuretic and antihypertensive agent that increases renal excretion of sodium, potassium, chloride, and bicarbonate ions by inhibiting tubular reabsorptive mechanisms.

Prorenoate is a steroidal aldosterone antagonist with potassium-sparing diuretic activity. Prorenoate antagonizes the activity of aldosterone at the mineralocorticoid receptor in the nephron and thereby prevents sodium reabsorption. This interferes with the sodium/potassium exchanger and causes sodium and water excretion while reducing potassium excretion.

The naturally-occurring estrogens are estrone , estradiol , and estriol . 16α-hydroxy Estrone (16α-OHE1) is a hydroxylated metabolite of E1 as well as an interconversion product with E2. E1 is 16α-hydroxylated by cytochrome P450 (CYP) isoforms, including CYP1A1, CYP3A5, CYP3A4, and CYP3A7, with CYP3A5 being breast-specific. 16α-OHE1 is sulphatized or glucuronidated before excretion. It is increased in rheumatoid arthritis and decreased by physical activity. Unlike the parent estrogens and other hydroxylated metabolites of E1, 16α-OHE1 binds covalently and persistently activates estrogen receptors. In addition, this metabolite increases cell proliferation and does not suppress TNF-α secretion, whereas other estrogen metabolites are not pro-proliferative and have marked effects on TNF-α secretion. The levels of 16α-OHE1 are increased in some forms of hormone therapy. Because hormone therapy increases breast cancer risk, 16α-OHE1 has been implicated as a risk factor for breast cancer, although supportive data remains elusive.

N-acetyl LTE4 is the major inactive metabolite of LTE4 found in bile. This route of metabolism is prominent in the rat, but of minor importance in humans. N-acetyl LTE4 is 100 times less potent than LTC4 as a vasoconstricting agent. In healthy human subjects urinary excretion of N-acetyl LTE4 is about 1.5 nmol/mol creatinine, which is considerably less than that of LTE4 (12 nmol/mol creatinine).

15-epiProstaglandin A1 (15-epiPGA1) is an R-stereoisomer of PGA1, belonging to the A-series prostaglandins derived from gorgonian soft corals. PGA1 is known for its effects on renal vasodilation, promoting sodium excretion through urine, and reducing arterial pressure in hypertensive individuals. However, the specific biological activities of 15-epiPGA1 have not yet been documented in published reports.

Thromboxane B2 (TXB2) is a compound significantly released from aggregating platelets and undergoes metabolic transformation during circulation into 11-dehydro TXB2 and 2,3-dinor TXB2. The latter, 2,3-dinor TXB2, serves as a prevalent urinary metabolite of TXB2 and acts as an indicator for in vivo TXA2 synthesis. Studies have shown that in healthy male volunteers, the median excretion rate of 2,3-dinor TXB2 is measured at 10.3 ng/hour, equivalent to 138 pg/mg of creatinine.

UNC569 (UNC 569) is a selective inhibitor of URAT1, a transporter in the kidney that regulates uric acid excretion from the body. It is also a selective uric acid re-absorption inhibitor. UNC569 could normalize the amount of uric acid excreted by gout patients previously classified as under-excretors.

Trichlormethiazide sodium is an orally active thiazide diuretic with antihypertensive effects. In an acute renal failure rats model, it increases urine volume (UV), Na and K excretion, and tends to improve creatinine clearance (CCRE).

MK-789 is an inhibitor of dehydropeptidase I. MK-789 and MK-791 alter the renal excretion of N-formimidoyl thienamycin from glomerular filtration plus tubular secretion to glomerular filtration only, possibly by competitively inhibiting the penetration of

P-CRESOL-d3 (METHYL-d3) is a deuterated compound of P-CRESOL. P-CRESOL has a CAS number of 106-44-5. p-Cresol (4-methylphenol) is a partially lipophilic moiety which strongly binds to plasma protein (close to 100%) under normal conditions. p-Cresol is metabolized through conjugation, mainly sulphation and glucuronization, but removal of the unconjugated p-cresol is, at least in part, via the urine. Therefore it is not surprising that this compound, together with several other phenoles, is retained when the kidneys fail. P-Cresol is an end-product of protein breakdown, and an increase of the nutritional protein load in healthy individuals results in enhanced generation and urinary excretion. The serum p-cresol concentration in uremic patients can be decreased by changing to a low-protein diet. p-Cresol is one of the metabolites of the amino acid tyrosine, and to a certain extent also of phenylalanine, which are converted to 4-hydroxyphenylacetic acid by intestinal bacteria, before being decarboxylated to p-cresol (putrefaction).

Uroguanylin-15 (Rat) is a bioactive natriuretic peptide hormone that regulates sodium excretion upon high NaCl intake by activating guanylate cyclase signaling pathways in the intestine and kidney. Initially isolated from rat urine and duodenum, it shares functional similarities with guanylin but has not been detected in rat colon extracts.