Category: 63208-82-2

Zearalenone induces endothelial cell apoptosis through activation of a cytosolic Ca²⁺/ERK1/2/p53/caspase 3 signaling pathway was written by Lee, Hyeon-Ju;Oh, Se-Young;Jo, Inho. And the article was included in Toxins in 2021.Category: thiazole The following contents are mentioned in the article:

Zearalenone (ZEN) is a mycotoxin that has been reported to damage various types of cells/tissues, yet its effects on endothelial cells (ECs) have never been investigated. Therefore, this study investigates the potential effects of ZEN using bovine aortic ECs (BAECs). In this study, we found that ZEN induced apoptosis of BAECs through increased cleavage of caspase 3 and poly ADP-ribose polymerase (PARP). ZEN also increased phosphorylation of ERK1/2 and p53, and treatment with the ERK1/2 or p53 inhibitor reversed ZEN-induced EC apoptosis. Transfection of BAECs with small interfering RNA against ERK1/2 or p53 revealed ERK1/2 as an upstream target of p53 in ZEN-stimulated apoptosis. ZEN increased the production of reactive oxygen species (ROS), yet treatment with the antioxidant did not prevent EC apoptosis. Similarly, blocking of estrogen receptors by specific inhibitors also did not prevent ZEN-induced apoptosis. Finally, chelation of cytosolic calcium (Ca²⁺) using BAPTA-AM or inhibition of endoplasmic reticulum (ER) Ca²⁺ channel using 2-APB reversed ZEN-induced EC apoptosis, but not by inhibiting ER stress using 4-PBA. Together, our findings demonstrate that ZEN induces EC apoptosis through an ERK1/2/p53/caspase 3 signaling pathway activated by Ca²⁺ release from the ER, and this pathway is independent of ROS production and estrogen receptor activation. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Category: thiazole).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles are a class of five-membered rings containing nitrogen and sulfur with excellent antitumor, antiviral and antibiotic activities. Electrophilic attack at nitrogen depends on the presence of electron density at nitrogen as well as the position and nature of substituent linked to the thiazole ring.Category: thiazole

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Pifithrin-α Inhibits Neural Differentiation of Newborn Cells in the Subgranular Zone of the Dentate Gyrus at Initial Stages of Audiogenic Kindling in Krushinsky-Molodkina Rat Strain was written by Kulikov, A. A.;Nasluzova, E. V.;Dorofeeva, N. A.;Glazova, M. V.;Lavrova, E. A.;Chernigovskaya, E. V.. And the article was included in Journal of Evolutionary Biochemistry and Physiology in 2021.Electric Literature of C16H19BrN2OS The following contents are mentioned in the article:

We hypothesized that a proapoptotic protein p53 can be one of the possible therapeutic targets in treating epilepsy and its neurodegenerative consequences. In the present work, we used the Krushinsky-Molodkina (KM) inbred rats, which are genetically prone to audiogenic seizures (AGS). Audiogenic kindling, a commonly accepted model of epileptogenesis, induces epileptiform activity in the limbic system and cerebral cortex. In KM rats, it has been shown that 4 AGS lead to an increase in proliferation, aberrant migration of newborn cells to the hilus, and accelerated neural differentiation of these cells. We revealed abnormalities neither in apoptosis nor in autophagy levels at the initial stages of temporal lobe (limbic) epilepsy. Treatment with pifithrin-α, a chem. p53 inhibitor, did not change apoptosis and autophagy levels but caused an increase in proliferation and migration of newborn cells to the granule cell layer of the dentate gyrus and to the hilus. However, a week after the last seizure, p53 inactivation entailed a decrease in the number of differentiating cells, as compared to the vehicle control group, despite a significant increase in the number of newborn cells. These data indicate a decrease in the neural differentiation rate of newborn cells, thus allowing pifitrin-α to be considered as a potential therapeutic agent to alleviate neurodegenerative disorders in epilepsy. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Electric Literature of C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles frequently appear in peptide studies. Thiazoles can also be used as protected formyl groups, which can be released in later stages of complex natural product synthesis. Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.Electric Literature of C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

MicroRNA -455-3p functions as a tumor suppressor by targeting HDAC2 to regulate cell cycle in hepatocellular carcinoma was written by Ma, Fuquan;Huang, Jin;Li, Weizhi;Li, Peijie;Liu, Mengying;Xue, Hui. And the article was included in Environmental Toxicology in 2022.Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide The following contents are mentioned in the article:

Hepatocellular carcinoma (HCC) is one of the most common cancers. MicroRNA has been studied more and more deeply and may become a new target for the treatment of HCC. Here, we investigated the role of miR-455-3p in HCC progression. Compared with non-tumor tissues and normal human hepatic cells, miR-455-3p expression was significantly downregulated in HCC tissues and cell lines. And overexpression of miR-455-3p inhibited cell proliferation and migration but promoted cell apoptosis in HCC cell lines HepG2 and Huh7. Mechanism studies displayed that miR-455-3p targeted HDAC2 and neg. regulated HDAC2 expression. Moreover, HDAC2 was highly expressed in HCC tissues and cell lines. Overexpression of HDAC2 reversed the inhibitory effects of miR-455-3p on cell proliferation, migration and cell cycle protein (CDK6 and cyclin D1) expression, and neutralized the promotion effects of miR-455-3p on cell apoptosis and the activation of p53 pathway. Furthermore, a p53 inhibitor Pifithrin-α (PFT-α) effectively abolished the effects of miR-455-3p on HCC cell behaviors. Addnl., the role of miR-455-3p in tumorigenesis was evaluated by using a mouse xenograft model, and the data showed that miR-455-3p suppressed tumor growth in vivo. In summary, our results suggested that miR-455-3p targeted HDAC2 to inhibit cell proliferation, migration and promote cell apoptosis via the activation of p53 pathway. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1). There are numerous natural products that possess a thiazole ring with broad pharmacological activities. Thiamine, also known as vitamin B1, possesses a thiazole ring linked with 2-methylpyrimidine-4-amine as hydrochloride salt.Quality Control of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

High COX-2 expression contributes to a poor prognosis through the inhibition of chemotherapy-induced senescence in nasopharyngeal carcinoma was written by Shi, Chen;Guan, Yongjun;Zeng, Liang;Liu, Guizhu;Zhu, Yinghong;Xu, He;Lu, Yichen;Liu, Jiabin;Guo, Jiaojiao;Feng, Xiangling;Zhao, Xinying;Jiang, Weihong;Li, Guancheng;Li, Guiyuan;Dai, Yun;Jin, Fengyan;Li, Wei;Zhou, Wen. And the article was included in International Journal of Oncology in 2018.Safety of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide The following contents are mentioned in the article:

Resistance to radiotherapy and chemotherapy currently represents one of the major reasons for therapeutic failure in nasopharyngeal carcinoma (NPC). However, the mechanisms underlying resistance to chemotherapy in NPC remain unclear. In this study, cell counting assay, cell cycle assay and senescence associated β-galactosidase activity were performed to evaluate cell growth, proliferation and senescence, resp. We found that the aberrant expression of cyclooxygenase-2 (COX-2) was associated with a poor outcome and recurrance in patients with NPC. In NPC cells, COX-2 overexpression increased cell proliferation, inhibited cellular senescence and resulted in chemoresistance, while the knockdown of COX-2 reduced cell proliferation, promoted cellular senescence and overcame chemoresistance. Furthermore, fibroblasts from COX-2 knockout mice exhibited cellular senescence, particularly when treated with chemotherapeutic agents. Mechanistically, COX-2 interacted with p53 protein and inhibited cellular senescence, which resulted in chemotherapeutic resistance. On the whole, these findings indicate that COX-2 may play a critical role in chemotherapeutic resistance in NPC via the inhibition of chemotherapy-induced senescence via the inactivation of p53. This study provides exptl. evidence for the preclin. value of increasing chemotherapy-induced senescence by targeting COX-2 as an effective antitumor treatment in patients with recurrent NPC. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Safety of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The higher aromaticity of thiazole is due to delocalization of a lone pair of sulfur electrons across the ring, which is evidenced by chemical shifts of ring hydrogen at δ 7.27 and 8.77 ppm (C2 and C4), indicating diamagnetic ring current. There are numerous natural products that possess a thiazole ring with broad pharmacological activities. Thiamine, also known as vitamin B1, possesses a thiazole ring linked with 2-methylpyrimidine-4-amine as hydrochloride salt.Safety of 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

MEHP/ethanol co-exposure favors the death of steatotic hepatocytes, possibly through CYP4A and ADH involvement was written by Tete, Arnaud;Gallais, Isabelle;Imran, Muhammad;Legoff, Louis;Martin-Chouly, Corinne;Sparfel, Lydie;Bescher, Maelle;Sergent, Odile;Podechard, Normand;Lagadic-Gossmann, Dominique. And the article was included in Food and Chemical Toxicology in 2020.Electric Literature of C16H19BrN2OS The following contents are mentioned in the article:

Liver steatosis has been associated with various etiol. factors (obesity, alc., environmental contaminants). How those factors work together to induce steatosis progression is still scarcely evaluated. Here, we tested whether phthalates could potentiate death of steatotic hepatocytes when combined with ethanol. Pre-steatotic WIF-B9 hepatocytes were co-exposed to mono (2-ethylhexyl) (MEHP, 500 nM; main metabolite of di (2-ethylhexyl) phthalate or DEHP) and ethanol (5 mM) for 5 days. An increased apoptotic death was detected, involving a DNA damage response. Using 4-Methypyrazole to inhibit ethanol metabolism, and CH-223191 to antagonize the AhR receptor, we found that an AhR-dependent increase in alc. dehydrogenase (ADH) activity was essential for cell death upon MEHP/ethanol co-exposure. Toxicity was also prevented by HET0016 to inhibit the cytochrome P 450 4A (CYP4A). Using the antioxidant thiourea, a role for oxidative stress was uncovered, notably triggering DNA damage. Finally, co-exposing the in vivo steatosis model of high fat diet (HFD)-zebrafish larvae to DEHP (2.56 nM)/ethanol (43 mM), induced the pathol. progression of liver steatosis alongside an increased Cyp4t8 (human CYP4A homolog) mRNA expression. Altogether, these results further emphasized the deleterious impact of co-exposures to ethanol/environmental pollutant towards steatosis pathol. progression, and unraveled a key role for ADH and CYP4A in such effects. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Electric Literature of C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles are a class of five-membered rings containing nitrogen and sulfur with excellent antitumor, antiviral and antibiotic activities. Thiazole is a versatile building block for the construction and lead generation of new drug discoveries. Numerous diazole-based compounds are in clinical use as anticancer, antileukemic, antiinflammatory, antiviral, antifungal, antirheumatic, immunomodulator, and antiparasitic agents.Electric Literature of C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Selective killing of human breast cancer cells by the styryl lactone (R)-goniothalamin is mediated by glutathione conjugation, induction of oxidative stress and marked reactivation of the R175H mutant p53 protein was written by Punganuru, Surendra R.;Madala, Hanumantha Rao;Arutla, Viswanath;Srivenugopal, Kalkunte S.. And the article was included in Carcinogenesis in 2018.Application of 63208-82-2 The following contents are mentioned in the article:

The mol. basis of anticancer and apoptotic effects of R-goniothalamin (GON), a plant secondary metabolite was studied. We show that induction of oxidative stress and reactivation of mutant p53 underlie the strong cytotoxic effects of GON against the breast cancer cells. Flow cytometry and other pertinent assays showed that GON-induced abundant reactive oxygen species (ROS), glutathione depletion, protein glutathionylation and activation of apoptotic markers. GON was found to conjugate with glutathione both in vitro and in cells and the product was characterized by mass spectrometry. We hypothesized that the redox imbalance induced by GON may affect the structure of the R175H mutant p53 protein, and account for greater cytotoxicity. Using the SKBR3 breast cancer and p53-null H1299 lung cancer cells stably expressing the R175H p53 mutant protein, we demonstrated that GON triggers the appearance of a wild-type-like p53 protein by using conformation-specific antibodies, immunoprecipitation, DNA-binding assays and target gene expression. p53 restoration was associated with a G2/M arrest, senescence, reduced cell migration, invasion and increased cell death. In SKBR3 xenografts developed in nude mice, there was a marked tumor growth delay by GON alone and GON + cisplatin combination. Our studies highlight the impact of tumor redox-stress generated by GON in activating the mutant p53 protein for greater antitumor efficacy. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Application of 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. Various laboratory methods exist for the organic synthesis of thiazoles. Prominent is the Hantzsch thiazole synthesis is a reaction between haloketones and thioamides.Application of 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Aqueous Extract of Sea Squirt (Halocynthia roretzi) with Potent Activity against Human Cancer Cells Acts Synergistically with Doxorubicin was written by Zhu, Yuting;Han, Shanhao;Li, Jianhui;Gao, Hongwei;Dong, Bo. And the article was included in Marine Drugs in 2022.Name: 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide The following contents are mentioned in the article:

Marine ascidian is becoming one of the main sources of an antitumor drug that has shown high bioactivity and extensive application in cancer treatment. Halocynthia roretzi, an edible marine sea squirt, has been demonstrated to have various kinds of biol. activities, such as anti-diabetic, anti-hypertension, and enhancing immunity. In this study, we reported that aqueous extracts from the edible parts of H. roretzi presented significantly inhibiting the efficiency on HepG-2 cell viability. The sep. mixed compound exhibited strong effects of inhibitory proliferation and induced apoptosis via the generation of ROS along with the concurrent loss of mitochondrial membrane potential on tumor cells. Furthermore, we found that there existed a significantly synergistic effect of the ascidian-extracted compound mixture with the anti-cancer drug doxorubicin. In the presence of the extracts from H. roretzi, the dose of doxorubicin at the cellular level could be reduced by a half dose. The extracts were further divided by semipreparative-HPLC and the active ingredients were identified as a mixture of fatty amide, which was composed of hexadecanamide, stearamide, and erucamide by UHPLC-MS/MS. Our results suggest that the potential toxicity of ascidian H. roretzi in tumor cells, and the compounds extracted from H. roretzi could be potentially utilized on functional nutraceuticals or as an adjunct in combination with chemotherapy. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Name: 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole rings are planar and aromatic. Thiazoles are characterized by larger pi-electron delocalization than the corresponding oxazoles and have therefore greater aromaticity. The nitrogen in thiazole is sp2 hybridized and the lone pair of electrons localized on the nitrogen is less reactive due to increased aromatic character and decreased basicity. It is protonated and alkylated/acylated at nitrogen forming hydrochloride and quaternary thiazolium salt.Name: 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

p53-Dependent pathway and the opening of mPTP mediate the apoptosis of co-cultured Sertoli-germ cells induced by microcystin-LR was written by Wu, Jinxia;Liu, Haohao;Huang, Hui;Yuan, Le;Liu, Chuanrui;Wang, Yueqin;Cheng, Xuemin;Zhuang, Donggang;Xu, Min;Chen, Xinghai;Losiewicz, Michael D.;Zhang, Huizhen. And the article was included in Environmental Toxicology in 2019.HPLC of Formula: 63208-82-2 The following contents are mentioned in the article:

In order to investigate the role and mechanisms of apoptosis (p53-dependent and mitochondrial pathways) of germ cells induced by MC-LR, the co-cultured primary Sertoli-germ cells from Sprague-Dawley rats were used for the experiments Expression levels of proteins, genes, and mitochondrial membrane potential (MMP) were obtained after exposing co-cultured Sertoli-germ cells to MC-LR with or without the addition of the p53 inhibitor, pifithrin-α (PFT-α), and MMP inhibitor, cyclosporin A (CsA). Results indicated that MC-LR could activate p53-dependent pathway-associated proteins in Sertoli-germ cells, leading to a decrease in MMP (indicating the opening of mitochondrial permeability transition pore [mPTP] and the release of Cytochrome-c [Cyt-c]) from the mitochondria into the cytoplasm and eventually the induction of apoptosis. PFT-α inhibited the expression ofp53, ameliorated the MMP of the co-cultured Sertoli-germ cells, and prevented the release of Cyt-c from the mitochondria into the cytoplasm, which reduces the occurrence of apoptosis. Similarly, the decreased release of Cyt-c from the mitochondria into the cytoplasm and the declined level of apoptosis in Sertoli-germ cells induced by MC-LR were observed after the addition of CsA. These results indicated that the apoptosis of the co-cultured Sertoli-germ cells induced by MC-LR was mediated by the p53-dependent pathway, with the involvement of the opening of mPTP. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2HPLC of Formula: 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1). Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.HPLC of Formula: 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Neuroprotective effects of pifithrin-α against traumatic brain injury in the striatum through suppression of neuroinflammation, oxidative stress, autophagy, and apoptosis was written by Huang, Ya-Ni;Yang, Ling-Yu;Greig, Nigel H.;Wang, Yu-Chio;Lai, Chien-Cheng;Wang, Jia-Yi. And the article was included in Scientific Reports in 2018.Computed Properties of C16H19BrN2OS The following contents are mentioned in the article:

Cortical and hippocampal neuronal damages caused by traumatic brain injury (TBI) are associated with motor and cognitive impairments; however, only little attention paid to the striatal damage. It is known that the p53 tumor-suppressor transcription factor participated in TBI-induced secondary brain damage. We investigated how the p53 inactivator pifithrin (PFT)-α affected TBI-induced striatal neuronal damage at 24 h post-injury. Sprague-Dawley rats subjected to a controlled cortical impact were used as TBI models. We observed that p53 mRNA significantly increased, whereas p53 protein expression was distributed predominantly in neurons but not in glia cells in striatum after TBI. PFT-α improved motor deficit following TBI. PFT-α suppressed TBI-induced striatal glial activation and expression of proinflammatory cytokines. PFT-α alleviated TBI-induced oxidative damage TBI induced autophagy was evidenced by increased protein expression of Beclin-1 and shift of microtubule-associated light chain (LC)3-I to LC3-II, and decreased p62. These effects were reduced by PFT-α. Post-injury PFT-α treatment reduced the number of degenerating (FJC-pos.) and apoptotic neurons. Our results suggest that PFT-α may provide neuroprotective effects via p53-dependent or -independent mechanisms depending on the cell type and timing after the TBI and can possibly be developed into a novel therapy to ameliorate TBI-induced neuronal damage. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Computed Properties of C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. Thiazole is a versatile building block for the construction and lead generation of new drug discoveries. Numerous diazole-based compounds are in clinical use as anticancer, antileukemic, antiinflammatory, antiviral, antifungal, antirheumatic, immunomodulator, and antiparasitic agents.Computed Properties of C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Connexin 32 deficiency protects the liver against ischemia/reperfusion injury was written by Wu, Shan;Yao, Weifeng;Chen, Chaojin;Chen, Huixin;Huang, Fei;Liu, Yiqian;Cai, Jun;Yuan, Dongdong;Hei, Ziqing. And the article was included in European Journal of Pharmacology in 2020.Synthetic Route of C16H19BrN2OS The following contents are mentioned in the article:

Hepatic ischemia/reperfusion (I/R) injury is a common complication in the clin. setting. Our previous study has shown that connexin 32 (Cx32) plays a major role in renal I/R injury; however, the role of Cx32 in hepatic I/R injury remains unknown. Liver tissue and serum samples from patients undergoing orthotopic liver transplantation (OLT) were used to evaluate the function of Cx32 in OLT post-reperfusion injury. Then, partial hepatic ischemia was established in global Cx32 knockout mice and wild-type mice followed by reperfusion. Hepatic injury markers were examined Cx32 small interfering RNA and the p53 inhibitor, pifithrin-α, tenovin-1 were used to examine the relationship between Cx32 and the p53/puma pathways in the BRL-3A and murine primary hepatocytes hypoxia/reoxygenation (H/R) model. Corresponding to liver damage, Cx32 was significantly induced both during OLT in human patients and partial hepatic I/R in mice. Cx32 KO mice exhibited less liver injury than controls. Cx32 deficiency significantly suppressed the p53/puma pathways and hepatocyte apoptosis. Similar results were observed in the BRL-3A and murine primary hepatocytes H/R model. Propofol protected against OLT post-reperfusion injury and hepatocyte apoptosis by inhibiting Cx32. In conclusion Cx32 is a novel regulator of hepatic I/R injury through the modulation of hepatocyte apoptosis and damage, largely via the p53/puma signaling pathway. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Synthetic Route of C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles are a class of five-membered rings containing nitrogen and sulfur with excellent antitumor, antiviral and antibiotic activities. Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.Synthetic Route of C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica