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Radiochemistry for Preclinical Imaging Studies
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Figure 16.22 gives a representative selection of the most popular chelating ligand systems for 68Ga applications. DTPA is an established chelator for radiometals. This system has been recently applied for labeling of pamoic acid with 68Ga as a necrosis marker (Prinsen et al. 2010). The macrocyclic DOTA served as a preferred binder for 68Ga in numerous peptide labeling protocols (Stasiuk and Long 2013). The heterobifunctional compound N,N′-bis[2-hydroxy-5-(carboxyethyl) benzyl]ethylenediamine-N,N′-diacetic acid (HBED-CC) was found to be superior to DOTA as the 68Ga complexing step occurred more efficient at room temperature (Eder et al. 2008). A related pyridine-based chelator suitable for chelation reaction at room temperature, H2DEDPA, has been reported by the group of Orvig et al. (Boros et al. 2012). The tripodal ligand CP256 is another promising new compound for rapid protein labeling under mild conditions (Berry et al. 2011).
Cytochrome c
Published in Robert A. Greenwald, CRC Handbook of Methods for Oxygen Radical Research, 2018
Any compound which reacts with O2− to give a product capable of directly reducing cytochrome c will, in effect, diminish the ability of SOD to inhibit cytochrome c reduction. Such compounds replace O2− with an SOD-insensitive reductant of the cytochrome c. When added to assay mixtures compounds with this property appear to inhibit SOD. Pamoic acid was shown to behave in this way.5
Hydrophobic ion pairing-based self-emulsifying drug delivery systems: a new strategy for improving the therapeutic efficacy of water-soluble drugs
Published in Expert Opinion on Drug Delivery, 2023
Jinghan Xin, Mengdi Qin, Genyang Ye, Haonan Gong, Mo Li, Xiaofan Sui, Bingyang Liu, Qiang Fu, Zhonggui He
Hydrophilic macromolecular drugs and lipophilic counterions forming HIP complexes are combined by charge attraction. The electrostatic interaction between the counterions and the macromolecules can be increased by optimizing the ratio, and thus the lipophilicity of the HIP complexes can also be improved [11,30]. The process is reversible, simple, and economical. Compared with lipidation methods those require covalent combination, HIP does not affect the structure and activity of molecules, and the natural charge of the drug is neutralized by the hydrophobic group of the counterion to increase lipophilicity [31–33]. For example, leuprolide, insulin, and bovine serum albumin were each paired with pamoic acid di-sodium salt for HIP complexes, whose log P increased by at least 2.5 units [24]. In another case, Miller and colleagues paired guanidino oseltamivir and zanamivir heptyl ester with 1-hydroxy-2-naphthoic acid respectively, and the lipophilicity increased by 3.7 units and 1.2 units [34]. Adequate lipophilicity enables increased encapsulation in the oil droplets of SEDDS and extends the drug release.
Comparison of triptorelin acetate vs triptorelin pamoate in the treatment of Central precocious puberty (CPP): a retrospective study
Published in Gynecological Endocrinology, 2020
Stefania Lasorella, Rossella Porto, Maria Laura Iezzi, Carmelo Pistone, Gian Luigi Marseglia, Alberto Verrotti, Ilaria Brambilla
Pamoic acid is considered for the FDA an inactive compound that allows long-acting formulations of numerous drugs; in particular, it has been shown to induce a G protein-coupled receptor 35 (GPR 35)-mediated phosphorylation of extracellular signaling with internalization of GPR35 and in mice, this is associated with a reduced visceral perception of pain. This suggests that pamoic acid has an unexpected biological function [21]. Furthermore, it has been shown that functional GPR35 are expressed by hippocampal neurons and influence neuronal activity [22]. Since the hippocampus is the site of pre-pubertal changes, a possible connection could be investigated.
An unusual complication of a long-acting injectable antipsychotic: deep venous thrombosis caused by olanzapine pamoate
Published in Psychiatry and Clinical Psychopharmacology, 2018
Serhat Tunç, Hamit Serdar Başbuğ
Olanzapine pamoate is an LAI form of olanzapine combined with the salt of the pamoic acid [17]. After injection into the gluteal muscle, the two components slowly dissociate into olanzapine and pamoic acid. The dissolution of the pamoic acid salt is slow, enabling a gradual release of olanzapine into the circulation over two to four weeks [18]. Other depot forms of LAI antipsychotics have a different mechanism to achieve the slow absorption. Most of the first-generation antipsychotics carry a terminal alcohol (-OH) which enables them to combine with carboxylic acids by esterification. However, the second-generation antipsychotics lack an alcohol (-OH) terminal suitable for esterification and present a different release mechanism. The dissemination thus occurs mainly by encapsulation of the drug into a degradable polymer (risperidone) and injection of a suspension of drug compound (olanzapine) [19]. The peak concentration of olanzapine pamoate is achieved in four days with a half-life of 26 days. Olanzapine plasma concentrations are sustained throughout two to four weeks of injection intervals [17]. This is an important pharmacokinetic feature as the timing of onset after injection is the primary concern for the clinician. Therefore, some strategies were recommended for the transition from oral to LAI form of olanzapine [18]. The starting LAI olanzapine dose should be 210 mg every two weeks or 405 mg every four weeks in patients who were stabilized with 10 mg of an oral dose. The dose may then be reduced after two months to a lower maintenance dose of 150 mg every two weeks or 300 mg every four weeks. For the patients who are stabilized with 15 and 20 mg of oral form, the initial LAI doses should be adjusted as 300 mg every two weeks. After two months, the maintenance doses then should be dropped to 210 mg every two weeks or 405 mg every four weeks in patients using 15 mg daily dose. However, the patients who are stabilized with 20 mg oral dose of olanzapine should remain at the level of 300 mg every two weeks as long as the clinical indication persists [20].