Thyrotropin-releasing hormone Chemical Properties

Melting point:

>143°C (dec.)

alpha 

-50 (D/25℃) (c=1.5, H2O)-65.5 (D) (c=1.0, H2O)

Boiling point:

494°C (rough estimate)

Density 

1.1675 (rough estimate)

refractive index 

1.6000 (estimate)

storage temp. 

−20°C

solubility 

H₂O: 10 mg/mL, clear, colorless

form 

powder

pka

13.05±0.20(Predicted)

color 

White to Off-White

PH

pH (10g/l, 25℃) : 3.0～4.0

Merck 

13,9663

BRN 

770238

Stability:

Hygroscopic

InChIKey

ITYONPBTNRIEBA-SRVKXCTJSA-N

CAS DataBase Reference

24305-27-9

Safety Information

Safety Statements 

22-24/25

WGK Germany 

2

RTECS 

TW3580000

F 

10-21

MSDS

• Language:English Provider:SigmaAldrich

Thyrotropin-releasing hormone Usage And Synthesis

Discovery

TRH was first isolated and characterized in 1969 by Roger Guillemin and Andrew Schally, who shared the Nobel Prize in Physiology or Medicine in 1977 “for their discoveries concerning the peptide hormone production of the brain.”The biosynthesis of TRH from a precursor molecule was first clarified in 1984 by isolation of a preproTRH cDNA from the skin of Xenopus laevis.  The structure of the TRH receptor (TRH-R) was first deduced from a cDNA isolated from the mouse pituitary in 1990.

Properties

Mr 362. Soluble in water, methanol, and ethanol; partially insoluble in chloroform; completely insoluble in ether and pyridine. Stable in solution at <15°C for more than a year; partially (1%) degraded at 40°C for 6 months. Resistant to proteolytic enzymes. Inactivated by diazotized sulfanilic acid (Pauly reagent). Plasma half-life is 2–6min.

Synthesis and release

TRH secretion is regulated by norepinephrine, histamine, dopamine, and serotonin. Cold-induced secretion of TSH from the rat anterior pituitary involves α-adrenergic regulation of TRH secretion. TRH neurons in the PVN are negatively regulated by thyroid hormones through a feedback mechanism. Locally produced T3 is taken by these neurons to regulate transcription, posttranslational modification, and degradation of TRH.

Gene, mRNA, and precursor

TRH is synthesized from a precursor that contains multiple copies of the TRH progenitor sequence GlnHis-Pro-Gly, which is flanked by dibasic cleavage sites at its N- and C-termini. The number of progenitor sequences in a precursor is diversified: six in humans, five in rats, four in chicken, seven in frogs, and six to eight in fish. Human preproTRH gene, TRH, location 3q13.3–q21, consists of three exons.

Clinical implications

The majority of thyroid disfunction is due to primary thyroid disease. On the other hand, central thyroid disfunction is related to a disorder of the pituitary (TSH), hypothalamus (TRH), or hypothalamic-pituitary portal circulation. Isolated central hypothyroidism was reported in a patient with inactivating mutations in the TRH-R gene.

Receptors

TRH-R is a seven-transmembrane-domain GPCR. Two major types of TRH-Rs (type I receptor including TRH-R1 and TRH-R3, and type II receptor [TRH-R2]), have been identified in vertebrates . Three and four subtypes of TRH-Rs have been identified in Xenopus laevis and teleost species, respectively. TRH action is mediated via a membrane receptor mainly coupled to Gq/11 protein. TRH induces the mobilization of intracellular Ca2+ and the activation of PKC in target cells.

Biological functions

The Trh knockout mice show normal development, but exhibit tertiary hypothyroidism and hyperglycemia due to diminished insulin secretion. The Trh knockout mice show defects in cerebellar long-term depression and a motor learning deficit.The Trhr1 knockout mice exhibit central hypothyroidism showing a decrease in serum T3, T4, and PRL levels but not in serum TSH levels. The Trhr1 knockout mice exhibit normal growth and development but displayed increased anxiety and depression levels. The Trhr2 knockout mice are euthyroid with normal serum TSH levels and exhibit normal development and growth. The mutant females exhibited moderately increased depression and reduced anxiety phenotypes.

Description

The first hypothalamic hypophysiotropic neurohormone identified, TRH consists of the tripeptide pGlu-His-ProNH2. It stimulates the secretion ofthyroid-stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH), and also functions as a neurotransmitter and neuromodulator.

Chemical Properties

White or yellowish-white powder, hygroscopic.

Uses

Thyrotropin-Releasing Hormone is a hypothalamic hypophysiotropic neuropeptide, which has the ability to stimulate the release of thyroid-stimulating hormone in mammals. It is proven that Thyrotropin-Releasing Hormone can be used to accelerate wound healing.

Uses

prothyrotropin

Indications

Thyrotropin-releasing hormone, or protirelin, consists of three amino acids. TRH (Relefact TRH) is used for tests to distinguish primary from secondary hypothyroidism.

Definition

ChEBI: Protirelin is a tripeptide composed of L-pyroglutamyl, L-histidyl and L-prolinamide residues joined in sequence. It has a role as a human metabolite. It is a peptide hormone and a tripeptide.

General Description

Thyrotropin releasing hormone (TRH) is a tripeptide hypothalamic regulatory hormone, encoded by the gene mapped to human chromosome 3q13.3-q21. TRH is expressed in a variety of organs including central nervous system (CNS) and gastrointestinal tract.

Biochem/physiol Actions

Thyrotropin releasing hormone (TRH) stimulates production and secretion of thyrotropin (TSH) and prolactin from the anterior pituitary. It also plays a vital role as a neurotransmitter and neuromodulator.

Clinical Use

TRH (200–500μg) administered intravenously to normal subjects causes a rise in TSH levels within 15–30min, resulting in an increase in T3 levels within 90–150min. In primary hypothyroidism, TSH hyperresponse to TRH occurs, with a typical elevation in the basal TSH levels. In secondary (pituitary) hypothyroidism, an impaired TSH response to TRH occurs, whereas in tertiary (hypothalamic) hypothyroidism normal or increased TSH response to TRH occurs. Protirelin is used to test the response of the anterior pituitary to TRH in people who may have medical conditions of thyroid function, including hyperthyroidism, Graves’ disease, and hypothyroidism. In addition, TRH has been used to assess the ability of the prolactin secretion in the pituitary.

Side effects

The peak TSH response to intravenous TRH occurs at 20 minutes. The mild and transient side effects, which occur only after intravenous TRH, include nausea, a flushing sensation, a desire to micturate, a peculiar taste, and tightness in the chest[1].

Thyrotropin-releasing hormone(24305-27-9)Related Product Information

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