The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy estrogens are produced from 2-OH estrogens through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH estrogens and particularly 2-Methoxy estrogens.

2-Methoxy estrogens has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy estrogen levels were lower in breast cancer patients than controls.

The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy estrogens are produced from 2-OH estrogens through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH estrogens and particularly 2-Methoxy estrogens.

2-Methoxy estrogens has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy estrogen levels were lower in breast cancer patients than controls.

2-Methoxyestrone is a key marker in the "FU Female FMV Urine Comprehensive Hormone" panel by Physicians Lab, playing a pivotal role in the assessment of estrogen metabolism and overall hormonal balance in women. It is a metabolite of estrone, one of the primary forms of estrogen in the body. The significance of 2-Methoxyestrone lies in its role as an indicator of how estrogen is being processed and metabolized within the body. This metabolite is often considered a "good" estrogen metabolite because it's associated with a lower risk of estrogen-related pathologies, including certain types of breast cancer.

The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy-E1 is produced from 2-OH-E1 through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH-E1 and particularly 2-Methoxy-E1.

2-Methoxy-E1 has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy-E1 levels were lower in breast cancer patients than controls.

The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy-E1 is produced from 2-OH-E1 through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH-E1 and particularly 2-Methoxy-E1.

2-Methoxy-E1 has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy-E1 levels were lower in breast cancer patients than controls.

2-Methyl-3-hydroxybutyric acid, which is also known as 3-Hydroxy-2-methyl-butanoic acid (HMBA) is a normal urinary metabolite involved in the isoleucine catabolism, as well as presumably beta-oxidation of fatty acids and ketogenesis, excreted in abnormally high amounts in beta-ketothiolase deficiency.

Beta-ketothiolase deficiency is an inherited disorder in which the body cannot effectively process a protein building block (amino acid) called isoleucine. This disorder also impairs the body's ability to process ketones, which are molecules produced during the breakdown of fats.

2-Methylacetoacetic acid is a metabolite that has an increased excretion in patients with acetoacetyl-CoA thiolase deficiency. Thiolases are ubiquitous and important enzymes. Several isoenzymes are known, which can occur in the cytosol, the mitochondria, or the peroxisomes. Thiolases are CoA-dependent enzymes which catalyze the formation of a carbon-carbon bond in a Claisen condensation step and its reverse reaction via a thiolytic degradation mechanism. Mitochondrial acetoacetyl-coenzyme A (CoA) thiolase (T2) is important in the pathways for the synthesis and degradation of ketone bodies as well as for the degradation of 2-methylacetoacetyl-CoA. Moreover, 2-methylacetoacetic acid is found to be associated with beta-ketothiolase deficiency, which is also an inborn error of metabolism. 2-Methylacetoacetic acid is found in urine and can be used as a biomarker for the diagnosis of beta-ketothiolase deficiency.

2-Methylcitric acid (MCA) is a vital biomarker for diagnosing and managing inherited metabolic disorders, particularly propionic acidemia (PA) and methylmalonic acidemia (MMA). This organic acid builds up when propionyl-CoA metabolism is disrupted, leading to its condensation with oxaloacetate through the action of citrate synthase.