(Des-L-threoninol8)-Octreotide amide
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(Des-L-threoninol8)-Octreotide amide

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

(Des-L-threoninol8)-Octreotide amide is a potential impurity of octreotide.

Category
Others
Catalog number
BAT-014747
CAS number
79486-60-5
Molecular Formula
C45H58N10O8S2
Molecular Weight
931.13
IUPAC Name
(4R,7S,10S,13S,16S,19R)-10-(4-aminobutyl)-19-[[(2S)-2-amino-3-phenylpropanoyl]amino]-16-benzyl-7-[(1R)-1-hydroxyethyl]-13-(1H-indol-3-ylmethyl)-6,9,12,15,18-pentaoxo-1,2-dithia-5,8,11,14,17-pentazacycloicosane-4-carboxamide
Synonyms
H-D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-NH2 (Disulfide bridge: Cys2-Cys7); D-Phenylalanyl-L-cysteinyl-L-phenylalanyl-D-tryptophyl-L-lysyl-L-threonyl-L-cysteinamide cyclic (2-7)-disulfide; (4R,7S,10S,13S,16S,19R)-10-(4-Aminobutyl)-16-benzyl-7-[(1R)-1-hydroxyethyl]-13-(1H-indol-3-ylmethyl)-6,9,12,15,18-pentaoxo-19-(L-phenylalanylamino)-1,2-dithia-5,8,11,14,17-pentaazacycloicosane-4-carboxamide
Appearance
Off-white Powder
Purity
≥95%
Density
1.4±0.1 g/cm3
Boiling Point
1378.1±65.0°C at 760 mmHg
Sequence
fCFwKTC-NH2 (Disulfide bridge: Cys2-Cys7)
Storage
Store at -20°C
Solubility
Soluble in Water
InChI
InChI=1S/C45H58N10O8S2/c1-26(56)38-45(63)53-36(39(48)57)24-64-65-25-37(54-40(58)31(47)20-27-12-4-2-5-13-27)44(62)51-34(21-28-14-6-3-7-15-28)42(60)52-35(22-29-23-49-32-17-9-8-16-30(29)32)43(61)50-33(41(59)55-38)18-10-11-19-46/h2-9,12-17,23,26,31,33-38,49,56H,10-11,18-22,24-25,46-47H2,1H3,(H2,48,57)(H,50,61)(H,51,62)(H,52,60)(H,53,63)(H,54,58)(H,55,59)/t26-,31+,33+,34+,35+,36+,37+,38+/m1/s1
InChI Key
PWRIWNRQEPOGNP-DYDSHOKNSA-N
Canonical SMILES
CC(C1C(=O)NC(CSSCC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)N1)CCCCN)CC2=CNC3=CC=CC=C32)CC4=CC=CC=C4)NC(=O)C(CC5=CC=CC=C5)N)C(=O)N)O
1. Cluster headache
Manjit Matharu BMJ Clin Evid. 2010 Feb 9;2010:1212.
Introduction: The revised International Headache Society (IHS) criteria for cluster headache are: attacks of severe or very severe, strictly unilateral pain, which is orbital, supraorbital, or temporal pain, lasting 15 to 180 minutes and occurring from once every other day to eight times daily. Methods and outcomes: We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of interventions to abort cluster headache? What are the effects of interventions to prevent cluster headache? We searched: Medline, Embase, The Cochrane Library, and other important databases up to June 2009 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations, such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA). Results: We found 23 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions. Conclusions: In this systematic review, we present information relating to the effectiveness and safety of the following interventions: baclofen (oral); botulinum toxin (intramuscular); capsaicin (intranasal); chlorpromazine; civamide (intranasal); clonidine (transdermal); corticosteroids; ergotamine and dihydroergotamine (oral or intranasal); gabapentin (oral); greater occipital nerve injections (betamethasone plus xylocaine); high-dose and high-flow-rate oxygen; hyperbaric oxygen; leuprolide; lidocaine (intranasal); lithium (oral); melatonin; methysergide (oral); octreotide (subcutaneous); pizotifen (oral); sodium valproate (oral); sumatriptan (oral, subcutaneous, and intranasal); topiramate (oral); tricyclic antidepressants (TCAs); verapamil; and zolmitriptan (oral and intranasal).
2. Home management of pediatric sulfonylurea ingestions
Courtney Temple, Ruby Hoang, Shana Kusin Clin Toxicol (Phila). 2022 Nov;60(11):1235-1239. doi: 10.1080/15563650.2022.2125875. Epub 2022 Oct 25.
Introduction: Sulfonylureas are oral antidiabetic medications that act by stimulating insulin release from pancreatic beta cells. Unintentional pediatric ingestions may result in hypoglycemia. While guidelines often recommend up to a 24-hour hospital observation period for any ingestion, the Oregon Poison Center has historically managed select patients at home. This study aimed to describe outcomes of home-managed pediatric sulfonylurea exposures and characteristics of ingestions that are appropriate for home monitoring. Methods: This is a retrospective chart review of pediatric (≤5 years) sulfonylurea ingestions in a single poison center over a 19-year period (2002-2020). We reviewed 491 individual cases for age, ingestion quantity, witnessed or unwitnessed ingestions, hypoglycemia (<60 mg/dL), disposition, and severe events (seizures or coma). We excluded cases in which missing pills were later found or another agent was identified. Results: Of 474 patients meeting inclusion criteria, 135 (28%) were initially managed at home. Of these, 115 (85.3%) were ingestions of ≤1 tablet, where 68 (59%) were witnessed and 47 (41%) were unwitnessed. One hundred twenty five (92.6%) of these patients were successfully monitored at home, with 10 (7%) ultimately referred to a healthcare facility (HCF). Symptoms of hypoglycemia, measured glucose on home meter <60 mg/dL, fluctuations in monitored glucose, or parental concern were indications for HCF referral. Of those referred, 5 (4%) developed uncomplicated, asymptomatic hypoglycemia. Two of these received octreotide, at the discretion of the treating physician. No patients developed seizures or coma. Discussion: We report 135 pediatric sulfonylurea ingestions managed with initial home monitoring, the majority of which were successfully monitored at home without any reported adverse events. Ten patients "failed home monitoring," as defined by referral to a healthcare facility. Of these, five developed hypoglycemia, though no patients developed symptoms or serious adverse events. Conclusion: Our findings support home observation for children ≤5 years with small ingestions of second-generation sulfonylureas.
3. A retrospective observational study on cases of anaplastic brain tumors treated with the Di Bella Method: A rationale and effectiveness
Giuseppe Di Bella, Vittoria Borghetto, Elena Costanzo Neuro Endocrinol Lett. 2021 Nov 30;42(7):464-483.
Despite all the new developments in cancer therapy, the life expectancy of patients with malignant anaplastic brain tumors and glioblastoma multiform (GBM) remains short. Since the establishment of the Di Bella Method (DBM) in cancer therapy, DBM was able to increase the survival rate and life quality, without overt toxicity, in comparison to what is described in the literature related to the analogous brain tumors, with the same immunohistochemical, histologic and clinical features. Therefore, we treated seven patients with malignant anaplastic brain tumors using the DBM protocol. DBM therapy consists of somatostatin and analogous (octreotide) all trans-retinoic acid (ATRA), β-Carotene, axerophthol dissolved in vitamin E, vitamin D, vitamin C, melatonin (MLT), proteoglycans-glycosaminoglycans, valproic acid, acetazolamide, diethyldithiocarbamate, hydroxyurea, and temozolomide. These molecules have either antiproliferative, antiangiogenic, cytostatic, antioxidant, antimetastatic (differentiative), and immunomodulating features. Moreover, the inclusion of ATRA, MLT, and glucosamine with sodium valproate, diethyldithiocarbamate and acetazolamide has reinforced antitumor properties of the therapy by extending them to cancer stem cells. Furthermore, the non-cytolytic and non-cytotoxic metronomic dosage of hydroxyurea and temozolomide had increased the DBM therapy outcome by strengthening anti-tumor capability. The results of such treatment revealed that all seven patients were still alive after 5 to 8 years of starting DBM. In conclusion, the multi-strategic objectives of DBM are inhibiting the proliferative-invasiveness and neoplastic angiogenesis, silencing the survival system of cancer stem cells, enhancing the immunomodulatory and antioxidant activities, improving vitality and efficiency of normal cells, and depressing the efficiency and vitality of neoplastic ones.
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