N-Acetyltyrosine is an acetylated derivative of the amino acid L-tyrosine. Ordinary L-tyrosine is less stable and also less soluble in water, which may result in reduced bioavailability. Acetylation enhances the solubility and stability of certain amino acids. N-Acetyltyrosine is commonly used in place of tyrosine in parenteral nutrition. It converts to tyrosine and then can be used in neurotransmitter treatment as a precursor of cathecholamine. N-Acetyltyrosine supports brain function by supporting the synthesis of the catecholamines norepinephrine and dopamine (neurotransmitters). N-Acetyltyrosine supplements are used to improve memory and cognitive performance in humans while they are experiencing psychological stress.

Aplidin (plitidepsin) is an investigative anticancer agent under development by PharmaMar, a pharmaceutical company that commercializes anticancer drugs of marine origin. Aplidin is isolated from the sea squirt (Aplidium albicans) and has shown anti-myeloma activity even in myelomas resistant to other agents. The drug has received orphan drug designation in the U.S., the European Union, and Switzerland. The target of plitidepsin is the eEF1A2 protein. The bonding of plitidepsin to this protein blocks its pro-oncogenic property and impedes the transportation of the misfolded proteins, which are toxic to the tumor, to the proteasome for their destruction. It also inhibits the activation of the aggresome by eEF1A2 and the destruction of the aggresome in the lysosome. This provokes anexcess of misfolded proteins, this causing cell death through apoptosis. Recently, a Phase III randomized trial in patients with relapsed/refractory multiple myeloma reported outcomes for plitidepsin plus dexamethasone compared with dexamethasone. Median progression-free survival was 3.8 months in the plitidepsin arm and 1.9 months in the dexamethasone arm. However, on 14 December 2017, the Committee for Medicinal Products for Human Use (CHMP) adopted a negative opinion, recommending the refusal of the marketing authorisation for the medicinal product Aplidin, intended for the treatment of multiple myeloma. At the time of the initial review, the CHMP was concerned that the data from the main study showed only a modest increase of around one month in the time patients given Aplidin lived without their disease getting worse, compared with those treated with dexamethasone alone. In addition, improvement in overall survival (how long patients lived overall) was not sufficiently demonstrated. Regarding safety, severe side effects were reported more frequently with the combination of Aplidin and dexamethasone than with dexamethasone alone. Based on the above, the CHMP was of the opinion that the benefits of Aplidin did not outweigh its risks and recommended that it be refused marketing authorisation.After re-examination, the Committee remained of the same opinion. The CHMP therefore confirmed its recommendation that the marketing authorisation be refused.

Atosiban (brand name Tractocile) is a competitive antagonist of human oxytocin at receptor level. In rats and guinea pigs, atosiban was shown to bind to oxytocin receptors, to decrease the frequency of contractions and the tone of the uterine musculature, resulting in a suppression of uterine contractions. Atosiban was also shown to bind to the vasopressin receptor, thus inhibiting the effect of vasopressin. Tractocile is indicated to delay imminent pre-term birth in pregnant adult women with: − regular uterine contractions of at least 30 seconds duration at a rate of ≥ 4 per 30 minutes − a cervical dilation of 1 to 3 cm (0-3 for nulliparas) and effacement of ≥ 50% − a gestational age from 24 until 33 completed weeks − a normal foetal heart rate. Atosiban does not have U.S. Food and Drug Administration (FDA) approval for use in the United States.

Methyldopa is an aromatic-amino-acid decarboxylase inhibitor in animals and in man. Methyldopa is a medication that has been used to treat high blood pressure since the 1960s. Methyldopa is indicated in the treatment of moderate to severe hypertension, including that complicated by renal disease. Only methyldopa, the L-isomer of alpha-methyldopa, has the ability to inhibit dopa decarboxylase and to deplete animal tissues of norepinephrine. D-isomer is relatively inactive. In man the antihypertensive activity appears to be due solely to the L-isomer, which became generally known as methyldopa (Aldomet). About twice the dose of the racemate (Methyldopa anhydrous, (±)-; DL-alpha-methyldopa) is required for equal antihypertensive effect. Racemic alpha-methyldopa was shown to be much less effective or ineffective for the treatment of hypertension. The comparative study of the hypotensive effect of L-alpha-methyl-dopa (L-isomer) versus the racemic form was performed. The short-term hypotensive effects of the racemic form and the L-isomer of alpha-methyl-dopa were compared in 13 hospitalized patients with arterial hypertension. After a placebo period the active preparations in a fixed dose of 1.5 g daily were administered for three-day periods separated by a second placebo period of three days, the sequence of the active drugs being alternated. Both substances were shown to exert significant hypotensive effects. The L-isomer produced significant blood-pressure reductions irrespective of whether or not it was given first, whereas the racemic form was effective only when given first. The blood-pressure levels obtained with the L-isomer were throughout lower than those with the racemic form. Methyldopa is a centrally acting antihypertensive agent. It is metabolized to alpha-methylnorepinephrine in the brain, and this compound is thought to activate central alpha-2 adrenergic receptors

18F-FET (18F-Fluoroethyl-L-tyrosine) is a radiolabelled amino acid. It penetrates the blood-brain barrier by a specific amino acid transport system. In the brain, it is taken up into upregulated tumoral cells but not incorporated into proteins. It is used as a biomarker for positron emission tomography for imaging brain tumors, where it has higher specificity than 18F-FDG.

Dibromotyrosine is a brominated derivative of a natural amino acid tyrosine. In the human body, dibromotyrosine is produced by eosinophil peroxidase secreted from activated eosinophils. Dibromotyrosine is naturally produced by marine sponges. Dibromotyrosine is used in medicine for the treatment of functional hyperthyroidisms. It acts by competing with iodination of tyrosines, thus reducing the active form of the thyroid hormones. Dibromotyrosine also appears to maintain the ability to control TSH production through negative feedback on the pituitary gland, reducing the biological activity of the thyroid. Dibromotyrosine is marketed in Italy under tradename Bromotiren.

Diiodotyrosine (DIT) is a regulatory ligand for thyroid peroxidase, enzyme, which is involved in the production of thyroxine (T4) and triiodothyronine (T3), the thyroid hormones. Diiodotyrosine was proposed to be a new marker of leukocyte phagocytic activity in sepsis and severe infections.