PIT 1CAS# 53501-41-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 53501-41-0 | SDF | Download SDF |
| PubChem ID | 3664359 | Appearance | Powder |
| Formula | C14H10ClN3O4S | M.Wt | 351.76 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble to 75 mM in DMSO | ||
| Chemical Name | N-[(3-chloro-2-hydroxy-5-nitrophenyl)carbamothioyl]benzamide | ||
| SMILES | C1=CC=C(C=C1)C(=O)NC(=S)NC2=CC(=CC(=C2O)Cl)[N+](=O)[O-] | ||
| Standard InChIKey | RIGXBXPAOGDDIG-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C14H10ClN3O4S/c15-10-6-9(18(21)22)7-11(12(10)19)16-14(23)17-13(20)8-4-2-1-3-5-8/h1-7,19H,(H2,16,17,20,23) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Selective PIP3 antagonist. Blocks the binding of PIP3 to the pleckstrin homology (PH) domain of Akt (IC50 = 31.03 μM). Inhibits cancer cell survival and induces apoptosis by inhibition of PIP3-dependent PI 3-kinase/Akt signaling. Exhibits antitumor activity in vivo. |
PIT 1 Dilution Calculator
PIT 1 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.8428 mL | 14.2142 mL | 28.4285 mL | 56.8569 mL | 71.0712 mL |
| 5 mM | 0.5686 mL | 2.8428 mL | 5.6857 mL | 11.3714 mL | 14.2142 mL |
| 10 mM | 0.2843 mL | 1.4214 mL | 2.8428 mL | 5.6857 mL | 7.1071 mL |
| 50 mM | 0.0569 mL | 0.2843 mL | 0.5686 mL | 1.1371 mL | 1.4214 mL |
| 100 mM | 0.0284 mL | 0.1421 mL | 0.2843 mL | 0.5686 mL | 0.7107 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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A Novel Clinical Entity of Autoimmune Endocrinopathy: Anti-PIT-1 Antibody Syndrome.[Pubmed:28245453]
Front Horm Res. 2017;48:76-83.
Pituitary-specific transcription factor 1 (PIT-1; POU domain, class 1, transcription factor 1 (POU1F1)) is an essential transcription factor for the differentiation of somatotrophs, lactotrophs, and thyrotrophs, and for the expression of growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH). Mutations in PIT-1 cause congenital defects in GH and PRL secretion and severe TSH insufficiency. Anti-PIT-1 antibody syndrome, firstly reported in 2011, is characterized by acquired GH, PRL, and TSH deficiencies without PIT-1 mutation and is associated with the presence of the circulating antibody against PIT-1 protein as a marker. Various autoantibodies are detected with multiple endocrine organopathies in this syndrome; therefore, it meets the criteria of autoimmune polyglandular syndrome. Mechanistically, cytotoxic T lymphocytes specifically reacting with PIT-1 protein play an important role in the development of this syndrome.
Combined pituitary hormone deficiency due to gross deletions in the POU1F1 (PIT-1) and PROP1 genes.[Pubmed:28356564]
J Hum Genet. 2017 Aug;62(8):755-762.
Pituitary development depends on a complex cascade of interacting transcription factors and signaling molecules. Lesions in this cascade lead to isolated or combined pituitary hormone deficiency (CPHD). The aim of this study was to identify copy number variants (CNVs) in genes known to cause CPHD and to determine their structure. We analyzed 70 CPHD patients from 64 families. Deletions were found in three Turkish families and one family from northern Iraq. In one family we identified a 4.96 kb deletion that comprises the first two exons of POU1F1. In three families a homozygous 15.9 kb deletion including complete PROP1 was discovered. Breakpoints map within highly homologous AluY sequences. Haplotype analysis revealed a shared haplotype of 350 kb among PROP1 deletion carriers. For the first time we were able to assign the boundaries of a previously reported PROP1 deletion. This gross deletion shows strong evidence to originate from a common ancestor in patients with Kurdish descent. No CNVs within LHX3, LHX4, HESX1, GH1 and GHRHR were found. Our data prove multiplex ligation-dependent probe amplification to be a valuable tool for the detection of CNVs as cause of pituitary insufficiencies and should be considered as an analytical method particularly in Kurdish patients.
