Day: November 22, 2022

Overexpression of p53 accelerates puberty in high-fat diet-fed mice through Lin28/let-7 system was written by Chen, Ting;Chen, Cailong;Wu, Haiying;Chen, Xiuli;Xie, Rongrong;Wang, Fengyun;Sun, Hui;Chen, Linqi. And the article was included in Experimental Biology and Medicine in 2021.Product Details of 63208-82-2 The following contents are mentioned in the article:

High fat intake is one of the most important reasons of the surging prevalence of childhood obesity all over the world. Obesity and high fat intake have been revealed to cause premature activation of hypothalamo-pituitary-gonadal axis and central precocious puberty. The onset of puberty is controlled by neuroendocrine mechanisms containing overlapping and interacting gene networks. The latter contains five major transcriptional level hubs, among which the transcriptional factor p53, a well-established tumor suppressor protein, also plays a crucial role in obesity and metabolic disorders. In the current study, we repeated prior observations that high-fat diet advances vaginal opening in rodents and extended these findings by demonstrating that high-fat diet mice had higher expression of p53 in hypothalami than mice fed with normal chow. More importantly, in high-fat diet mice, hypothalamus-specific overexpression of p53 can make vaginal opening much earlier, while inhibition of p53 expression relatively delayed vaginal opening. The c-Myc and Lin28b levels increased, while let-7a mRNA levels decreased in the high-fat diet mice. Overexpression of p53 reduced c-Myc and Lin28b mRNA and protein levels, whereas elevated let-7a mRNA levels in high-fat diet mice. Inhibition of p53 expression by pifithrin-a elevated c-Myc and Lin28b but reduced let-7a levels in high-fat diet mice. In conclusion, high fat intake can accelerate the onset of puberty by up-regulation of p53 expression in hypothalamus. Overexpressed p53 may accelerate hypothalamo-pituitary-gonadal axis activation partially through the c-Myc/Lin28/let-7 system. Impact statement: High-fat intake and subsequent obesity are associated with premature onset of puberty, but the exact neuroendocrine mechanisms are still unclear. The transcriptional factor p53 has been predicted to be a central hub of the gene networks controlling the pubertal onset. Besides, p53 also plays crucial roles in metabolism Here, we explored p53 in the hypothalami of mice fed a high-fat diet (HFD), which showed an up-regulated expression. Besides, we also revealed that overexpressed p53 may accelerate hypothalamo-pituitary-gonadal (HPG) axis activation partially through the c-Myc/Lin28/let-7 system. These results can deepen our understanding of the interaction between metabolic regulation and puberty onset control, and may shed light on the neuroendocrine mechanisms of obesity-related central precocious puberty. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Product Details 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. Thiazoles are a class of five-membered rings containing nitrogen and sulfur with excellent antitumor, antiviral and antibiotic activities.Various laboratory methods exist for the organic synthesis of thiazoles. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.Product Details of 63208-82-2

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

Inhibition of mTOR Signaling Enhances Maturation of Cardiomyocytes Derived From Human-Induced Pluripotent Stem Cells via p53-Induced Quiescence was written by Garbern, Jessica C.;Helman, Aharon;Sereda, Rebecca;Sarikhani, Mohsen;Ahmed, Aishah;Escalante, Gabriela O.;Ogurlu, Roza;Kim, Sean L.;Zimmerman, John F.;Cho, Alexander;MacQueen, Luke;Bezzerides, Vassilios J.;Parker, Kevin Kit;Melton, Douglas A.;Lee, Richard T.. And the article was included in Circulation in 2020.Related Products of 63208-82-2 The following contents are mentioned in the article:

Background: Current differentiation protocols to produce cardiomyocytes from human induced pluripotent stem cells (iPSCs) are capable of generating highly pure cardiomyocyte populations as determined by expression of cardiac troponin T. However, these cardiomyocytes remain immature, more closely resembling the fetal state, with a lower maximum contractile force, slower upstroke velocity, and immature mitochondrial function compared with adult cardiomyocytes. Immaturity of iPSC-derived cardiomyocytes may be a significant barrier to clin. translation of cardiomyocyte cell therapies for heart disease. During development, cardiomyocytes undergo a shift from a proliferative state in the fetus to a more mature but quiescent state after birth. The mechanistic target of rapamycin (mTOR)-signaling pathway plays a key role in nutrient sensing and growth. We hypothesized that transient inhibition of the mTOR-signaling pathway could lead cardiomyocytes to a quiescent state and enhance cardiomyocyte maturation. Methods: Cardiomyocytes were differentiated from 3 human iPSC lines using small mols. to modulate the Wnt pathway. Torin1 (0 to 200 nmol/L) was used to inhibit the mTOR pathway at various time points. We quantified contractile, metabolic, and electrophysiol. properties of matured iPSC-derived cardiomyocytes. We utilized the small mol. inhibitor, pifithrin-α, to inhibit p53 signaling, and nutlin-3a, a small mol. inhibitor of MDM2 (mouse double minute 2 homolog) to upregulate and increase activation of p53. Results: Torin1 (200 nmol/L) increased the percentage of quiescent cells (G0 phase) from 24% to 48% compared with vehicle control (P<0.05). Torin1 significantly increased expression of selected sarcomere proteins (including TNNI3 [troponin I, cardiac muscle]) and ion channels (including Kir2.1) in a dose-dependent manner when Torin1 was initiated after onset of cardiomyocyte beating. Torin1-treated cells had an increased relative maximum force of contraction, increased maximum oxygen consumption rate, decreased peak rise time, and increased downstroke velocity. Torin1 treatment increased protein expression of p53, and these effects were inhibited by pifithrin-α. In contrast, nutlin-3a independently upregulated p53, led to an increase in TNNI3 expression and worked synergistically with Torin1 to further increase expression of both p53 and TNNI3. Conclusions: Transient treatment of human iPSC-derived cardiomyocytes with Torin1 shifts cells to a quiescent state and enhances cardiomyocyte maturity. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Related Products 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. The thiazole ring has been identified as a central feature of numerous natural products, perhaps the most famous example of which is epothilone.Various laboratory methods exist for the organic synthesis of thiazoles. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.Related Products of 63208-82-2

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

Bacteria-propelled microtubular motors for efficient penetration and targeting delivery of thrombolytic agents was written by Xie, Songzhi;Mo, Chuanfei;Cao, Wenxiong;Xie, Shuang;Li, Shang;Zhang, Zhanlin;Li, Xiaohong. And the article was included in Acta Biomaterialia in 2022.Synthetic Route of C20H18N2O2S The following contents are mentioned in the article:

Effective thrombolysis is critical to rapidly rebuild blood flow for thrombosis patients. Drug delivery systems have been developed to address inadequate pharmacokinetics of thrombolytic agents, but challenges still remain in the timely removal of blood clots regarding the dense fibrin networks. Herein, rod-shaped tubular micromotors were developed to achieve efficient penetration and thorough destruction of thrombi. By using electrospun fiber fragments as the template, urokinase (uPA)-loaded polydopamine (PDA) microtubes with surface decorated fucoidan (FuPDAuPA) were prepared at the aspect ratio of around 2. One E. coli Nissle 1917 (EcN) was assembled into one microtube to construct a FuPDAuPA@EcN hybrid micromotor through PDA adhesion and L-aspartate induction. The pharmacokinetic anal. indicates that the encapsulation of uPA into micromotors extends the half-life from 0.4 to 5.6 h and increases the bioavailability over 10 times. EcN-propelled motion elevates adsorption capacities of FuPDAuPA@EcN for more than four times compared with that of FuPDAuPA. The fucoidan-mediated targeting causes 2-fold higher thrombolysis capacity in vitro and over 10-fold higher uPA accumulation in thrombi in vivo. In the treatment of venous thrombi at mouse hindlimbs, i.v. administration of FuPDAuPA@EcN completely removed blood clots with almost full recovery of blood flows and apparently alleviated tail bleeding. It should be noted that FuPDAuPA@EcN treatment at a reduced uPA dose caused no significant difference in the blood flow rate compared with those of FuPDAuPA. The synergistic action of fucoidan-induced targeting and EcN-driven motion provides a prerequisite for promoting thrombolytic efficacy and reducing uPA dose and bleeding side effect. The standard treatment to thrombosis patient is i.v. infusion of thrombolytic agents, but the associated bleeding complications and impairment of normal haemostasis greatly offset the therapeutic benefits. Drug delivery systems have been developed to address the limitations of inadequate pharmacokinetics of thrombolytic agents, but challenges still exist in less efficient penetration into dense networks for thorough destruction of thrombi. Up to now only few attempts have been made to construct nano-/micromotors for combating thrombosis and there is no single case that antithrombosis is assisted by bacteria or cells-propelled motors. Herein, bacteria-propelled microtubes were developed to carry urokinase for efficient penetration into blood clots and effective thrombolysis. The synergistic action of bacteria-driven motion and specific ligand-induced targeting holds a promising treatment strategy for life-threatening cardiovascular diseases such as thrombosis and atherosclerosis. This study involved multiple reactions and reactants, such as 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0Synthetic Route of C20H18N2O2S).

3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1). 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.Synthetic Route of C20H18N2O2S

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

Synthesis of some 4-alkoxy- and 6-alkoxy-2-benzo-thiazolylamides was written by Mndzhoyan, A. L.;Azaryan, A. S.;Iradyan, M. A.;Aroyan, A. A.. And the article was included in Azerbaidzhanskii Khimicheskii Zhurnal in 1967.Name: 6-Butoxybenzo[d]thiazol-2-amine The following contents are mentioned in the article:

o- and p-Alkoxynitrobenzenes are hydrogenated over Ni-Cr2O3 to give o- and p-alkoxyanilines (I). Treating I with KSCN and Br gave the corresponding II and III, resp., which were converted into the corresponding amides (IV) and (V), resp. Thus, a mixture of 0.3 mole alkoxynitrobenzene, 50 cc. EtOH, and 4 g. Ni-Cr2O3 catalyst was hydrogenated in an autoclave at 110-20°/100 atm. for 10-12 hrs., filtered, and distilled to give 74.8-86.3% I. From I the following II and III were prepared (R, m.p., m.p. hydrochloride, and % yield given): 6-Et, 159-60°, 199-200°, 60.9; 4-Et, 76-8°, 176-8°, 51.9; 6-Pr, 127-9°, 189-90°, 86.5; 6-iso-Pr, 158-9°, 191-3°, 80.2; 4-Pr, 114-15°, 160-1°, 51.2; 6-Bu, 119-21°, 140-1°, 89.6; 6-iso-Bu, 160-1°, 189-91°, 69.1. A mixture of 0.05 mole acyl chloride and 150 cc. 1:1 Me2CO-dioxane placed in a flask connected with extractor in which a paper extraction shell containing 0.1 mole II or III was placed, was heated on a water bath to complete solution of II or III, filtered, washed with Me2CO, and crystallized from EtOH to obtain the following IV (R, R1, m.p., and % yield given): Et, iso-PrCO, 91-2°, 45.5; Et, Bz, 109-10°, 80.5; Et, MeOC6H4CO (A), 120-2°, 85.3; Et, EtOC6H4CO (B), 116-18°, 76; Et, PrOC6H4CO (C), 94-7°, 84.1; Et, iso-PrOC6H4CO (D), 94-6°, 84.2; Et, BuOC6H4CO (E), 97-8°, 81; Et, PhSO2 (F), 155-7°, 87.4; Et, 2-furoyl (G), 129-30°, 83.3; Et, 2-benzofuroyl (H), 152-4°, 71.8; Et, 2-(2,3-dihydrobenzofuroyl) (I), 110-12°, 70.6; Pr, EtC6H4CO, 191-2°, 79; Pr, G, 224-5°, 80.9; Pr, I, 169-70°, 79.1; and the following V (same data): Et, PrCO, 172-3°, 53.3; Et, iso-PrCO, 140-1°, 45.4; Et, Bz, 222-5°, 87.2; Et, A, 198-200°, 86.9; Et, B, 212-13°, 70.1; Et, C, 224-6°, 84.7; Et, D, 197-200°, 73; Et, F, 199-202°, 60.1; Et, E, 202-3°, 68; Et, iso-BuOC6H4CO, 221-2°, 60; Et, G, 158-9°, 51.9; Et, H, 216-17°, 64.6; Et, I, 142-3°, 90.5; Pr, Bz, 220-2°, 69.2; Pr, A, 145-6°, 80; Pr, B, 204-6°, 86.8; Pr, C, 192-4°, 81.1; Pr, D, 189-90°, 91.8; Pr, E, 197-8°, 67.9; Pr, F, 200-2°, 85.4; Pr, G, 151-2°, 79.5; Pr, H, 212-13°, 65.3; Pr, I, 120-1°, 73.4; iso-Pr, iso-PrCO, 136-9°, 40.3; iso-Pr, BuCO, 138-40°, 49; iso-Pr, Bz, 225-6°, 83.7; iso-Pr, A, 228-9°, 73.1; iso-Pr, B, 215-16°, 60; iso-Pr, F, 255-6°, 68.8; iso-Pr, G, 181-4°, 58.6; Bu, BuCO, 140-1°, 70.6; Bu, Bz, 184-6°, 84.6; Bu, A, 181-2°, 50.1; Bu, B, 182-4°, 81.1; Bu, E, 195-7°, 69.8; Bu, H, 158-60°, 76.5; iso-Bu, A, 222-3°, 85.1; Et, ClCH2CO, 170-1°, 81.4; Bu, ClCH2CO, 172-3°, 70.4. A mixture of 0.03 mole Et2NH, 25 cc. EtOH, 0.01 mole (N-6-alkoxy-2-benzothiazolyl)-2-chloroacetamide, and 25 cc. EtOH was heated on a water bath 2-3 hrs., EtOH was distilled, the residue alkalized with 10% NaHCO3 and extracted with Et2O, the extract dried with Na2SO4 and distilled to give the corresponding V: (R, R1, b.p./mm., m.p., and % yield given): Et, Et2NCH2CO, 218-20°/5, 90-2°, 31.9; Bu, Et2NCH2CO, 130-3°/5, 121-2°, 48.3. This study involved multiple reactions and reactants, such as 6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7Name: 6-Butoxybenzo[d]thiazol-2-amine).

6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7) 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. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.Name: 6-Butoxybenzo[d]thiazol-2-amine

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

Synthesis of some 4-alkoxy- and 6-alkoxy-2-benzo-thiazolylamides was written by Mndzhoyan, A. L.;Azaryan, A. S.;Iradyan, M. A.;Aroyan, A. A.. And the article was included in Azerbaidzhanskii Khimicheskii Zhurnal in 1967.Application In Synthesis of 6-Isopropoxybenzo[d]thiazol-2-amine The following contents are mentioned in the article:

o- and p-Alkoxynitrobenzenes are hydrogenated over Ni-Cr2O3 to give o- and p-alkoxyanilines (I). Treating I with KSCN and Br gave the corresponding II and III, resp., which were converted into the corresponding amides (IV) and (V), resp. Thus, a mixture of 0.3 mole alkoxynitrobenzene, 50 cc. EtOH, and 4 g. Ni-Cr2O3 catalyst was hydrogenated in an autoclave at 110-20°/100 atm. for 10-12 hrs., filtered, and distilled to give 74.8-86.3% I. From I the following II and III were prepared (R, m.p., m.p. hydrochloride, and % yield given): 6-Et, 159-60°, 199-200°, 60.9; 4-Et, 76-8°, 176-8°, 51.9; 6-Pr, 127-9°, 189-90°, 86.5; 6-iso-Pr, 158-9°, 191-3°, 80.2; 4-Pr, 114-15°, 160-1°, 51.2; 6-Bu, 119-21°, 140-1°, 89.6; 6-iso-Bu, 160-1°, 189-91°, 69.1. A mixture of 0.05 mole acyl chloride and 150 cc. 1:1 Me2CO-dioxane placed in a flask connected with extractor in which a paper extraction shell containing 0.1 mole II or III was placed, was heated on a water bath to complete solution of II or III, filtered, washed with Me2CO, and crystallized from EtOH to obtain the following IV (R, R1, m.p., and % yield given): Et, iso-PrCO, 91-2°, 45.5; Et, Bz, 109-10°, 80.5; Et, MeOC6H4CO (A), 120-2°, 85.3; Et, EtOC6H4CO (B), 116-18°, 76; Et, PrOC6H4CO (C), 94-7°, 84.1; Et, iso-PrOC6H4CO (D), 94-6°, 84.2; Et, BuOC6H4CO (E), 97-8°, 81; Et, PhSO2 (F), 155-7°, 87.4; Et, 2-furoyl (G), 129-30°, 83.3; Et, 2-benzofuroyl (H), 152-4°, 71.8; Et, 2-(2,3-dihydrobenzofuroyl) (I), 110-12°, 70.6; Pr, EtC6H4CO, 191-2°, 79; Pr, G, 224-5°, 80.9; Pr, I, 169-70°, 79.1; and the following V (same data): Et, PrCO, 172-3°, 53.3; Et, iso-PrCO, 140-1°, 45.4; Et, Bz, 222-5°, 87.2; Et, A, 198-200°, 86.9; Et, B, 212-13°, 70.1; Et, C, 224-6°, 84.7; Et, D, 197-200°, 73; Et, F, 199-202°, 60.1; Et, E, 202-3°, 68; Et, iso-BuOC6H4CO, 221-2°, 60; Et, G, 158-9°, 51.9; Et, H, 216-17°, 64.6; Et, I, 142-3°, 90.5; Pr, Bz, 220-2°, 69.2; Pr, A, 145-6°, 80; Pr, B, 204-6°, 86.8; Pr, C, 192-4°, 81.1; Pr, D, 189-90°, 91.8; Pr, E, 197-8°, 67.9; Pr, F, 200-2°, 85.4; Pr, G, 151-2°, 79.5; Pr, H, 212-13°, 65.3; Pr, I, 120-1°, 73.4; iso-Pr, iso-PrCO, 136-9°, 40.3; iso-Pr, BuCO, 138-40°, 49; iso-Pr, Bz, 225-6°, 83.7; iso-Pr, A, 228-9°, 73.1; iso-Pr, B, 215-16°, 60; iso-Pr, F, 255-6°, 68.8; iso-Pr, G, 181-4°, 58.6; Bu, BuCO, 140-1°, 70.6; Bu, Bz, 184-6°, 84.6; Bu, A, 181-2°, 50.1; Bu, B, 182-4°, 81.1; Bu, E, 195-7°, 69.8; Bu, H, 158-60°, 76.5; iso-Bu, A, 222-3°, 85.1; Et, ClCH2CO, 170-1°, 81.4; Bu, ClCH2CO, 172-3°, 70.4. A mixture of 0.03 mole Et2NH, 25 cc. EtOH, 0.01 mole (N-6-alkoxy-2-benzothiazolyl)-2-chloroacetamide, and 25 cc. EtOH was heated on a water bath 2-3 hrs., EtOH was distilled, the residue alkalized with 10% NaHCO3 and extracted with Et2O, the extract dried with Na2SO4 and distilled to give the corresponding V: (R, R1, b.p./mm., m.p., and % yield given): Et, Et2NCH2CO, 218-20°/5, 90-2°, 31.9; Bu, Et2NCH2CO, 130-3°/5, 121-2°, 48.3. This study involved multiple reactions and reactants, such as 6-Isopropoxybenzo[d]thiazol-2-amine (cas: 15850-81-4Application In Synthesis of 6-Isopropoxybenzo[d]thiazol-2-amine).

6-Isopropoxybenzo[d]thiazol-2-amine (cas: 15850-81-4) 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.Application In Synthesis of 6-Isopropoxybenzo[d]thiazol-2-amine

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

Organic thiocyanates. XIX. Thiocyanation of phenol ethers was written by Pohloudek-Fabini, Roland;Luess, K. D.. And the article was included in Archives de Pharmacie (Paris) in 1966.Computed Properties of C11H14N2OS The following contents are mentioned in the article:

Thiocyanation of alkyl phenyl ethers with inorganic thiocyanates and Br gave low yields of thiocyanates because bromination occurred simultaneously. Alkyl aminophenyl ethers yielded mixtures of mono and dithiocyanato derivatives When heated or treated with acids, the o-aminothiocyanato derivatives isomerized to 2-aminobenzothiazoles. Unsubstituted alkyl thiocyanatophenyl ethers were prepared from the corresponding aminophenyl ethers by diazotization and treatment with KSCN, CuSCN, and CoCl2. Phenol ethers (0.1 mole) and 0.3 mole NaSCN or KSCN in AcOH, 100 g. NH4SCN in MeOH, or 0.5 mole NaSCN or KSCN in AcOMe were cooled and treated with 0.2 mole Br in the same solvent (compound used, product(s), m.p., and % yield in AcOH, MeOH, and AcOMe listed): PhOMe, 4-MeOC6H4SCN, 34-5°, 12, 0, -; PhOEt, 4-EtOC6H4SCN, 46-7.5°, 17, 0, -; PhOPr, 4-PrOC6H4SCN, 36-6.5°, 17, 0, -; PhOBu, 4-BuOC6H4SCN, 26-7°, 15, 0, -; o-anisidine, 1,2,5-MeO(H2N)C6H3SCN, 52-3°, 68, 41, 92; 1,2,3,5-MeO(H2N)C6H2(SCN)2, 101-3° and 233° (twice), 28, 56, 0, and 4-methoxy-6-thiocyanato-2-aminobenzothiazole, 233-5° (decomposition), 60, 0, 0; m-anisidine, 1,3,6-MeO(H2N)C6H3SCN, 109-11°, 39, 2, 22, and 1,3,4,6-MeO(H2N)C6H2(SCN)2, 155-7°, 84, 75, 47; p-anisidine, 1,4,3-MeO(H2N)C6H3SCN, 61-2 and 168°, 0, 0, 25, 6-methoxy-2-aminobenzothiazole, 169°, 91, 3, 3, and 6-methoxy-4-thiocyanato-2-aminobenzothiazole, 212-16° (decomposition), 15, 72, 0; o-phenetidine, 1,2,5-EtO(H2N)C6H3SCN, 82-3°, 79, 53, 75, and 1,2,3,5-EtO(H2N)C6H2(SCN)2, 103-6° and 228°, 30, 80, 0; m-phenetidine, 1,3,4,6-EtO(H2N)C6H2(SCN)2, 105-7.5°, 100, 100, 92; p-phenetidine, 1,4,3-EtO(H2N)C6H3SCN, 70-2 and 164°, 0, 0, 31, 6-ethoxy-2-aminobenzothiazole, 164-6, 89, 42, 0, and 6-ethoxy-4-thiocyanato-2-aminobenzothiazole, 206-12° (decomposition), 5, 31, 0; 1,4-PrOC6H4NH2, 6-propoxy-2-aminobenzothiazole, 137-9°, 67, 22, -; 1,4-BuOC6H4NH2, 6-butoxy-2-aminobenzothiazole, 120-1°, 26, 15, -. Thiocyanates prepared by diazotization were (starting material, product, m.p., and % yield listed): o-anisidine, 1,2-MeOC6H4SCN, – (b14 151-2°), 39; m-anisidine, 1,3-MeOC6H4SCN, – (b8 151-2°), 40; p-anisidine, 1,4-MeOC6H4SCN, 33-4°, 29; o-phenetidine, 1,2-EtOC6H4SCN, 23-4° (b7 122-31°), 14; m-phenetidine, 1,3-EtOC6H4SCN, – (b9 138-42°), 42; p-phenetidine, 1,4-EtOC6H4SCN, 44-6°, 17; 1,4-PrOC6H4NH2, 1,4-PrOC6H4NH2, 1,4-PrOC6H4SCN, 34-6° (b6 145°), 20; 1,4-BuOC6H4NH2, 1,4-BuOC6H4SCN, 25-6°, 25; 1,2,5-MeO(H2N)C6H3SCN, 1,2,5-MeOC6H3(SCN)2, 89-93.5°, 29; 1,2,3,5-MeO(H2N)C6H2(SCN)2, 1,2,3,5-MeOC6H2(SCN)3, 129-34°, 59; 1,3,4,6-MeO(H2N)C6H2(SCN)2, 1,3,4,6-MeOC6H2(SCN)3, 114-18.5°, 90 (putative); 1,3,4,6-EtO(H2N)C6H2(SCN)2, 1,3,4,6-EtOC6H2(SCN)3, 115-19°, 100 (putative); 4-methoxy-6-thiocyanato-2-aminobenzothiazole, 4-methoxy-2,6-dithiocyanobenzothiazole, 125-8°, 43; 6-methoxy-2-aminobenzothiazole, 6-methoxy-2-thiocyanobenzothiazole, 86-7°, 30; 6-ethoxy-2-aminobenzothiazole, 6-ethoxy-2-thiocyanatobenzothiazole, 84-8°, 80; 1,2,5-EtO(H2N)C6H3SCN, 1,2,5-EtOC6H3(SCN)2, 52-7°, 80 (putative). This study involved multiple reactions and reactants, such as 6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7Computed Properties of C11H14N2OS).

6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7) 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. 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.Computed Properties of C11H14N2OS

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

Solubilized ubiquinol for preserving corneal function was written by Naguib, Youssef W.;Saha, Sanjib;Skeie, Jessica M.;Acri, Timothy;Ebeid, Kareem;Abdel-rahman, Somaya;Kesh, Sandeep;Schmidt, Gregory A.;Nishimura, Darryl Y.;Banas, Jeffrey A.;Zhu, Min;Greiner, Mark A.;Salem, Aliasger K.. And the article was included in Biomaterials in 2021.Product Details of 38215-36-0 The following contents are mentioned in the article:

Defective cellular metabolism, impaired mitochondrial function, and increased cell death are major problems that adversely affect donor tissues during hypothermic preservation prior to transplantation. These problems are thought to arise from accumulated reactive oxygen species (ROS) inside cells. Oxidative stress acting on the cells of organs and tissues preserved in hypothermic conditions before surgery, as is the case for cornea transplantation, is thought to be a major reason behind cell death prior to surgery and decreased graft survival after transplantation. We have recently discovered that ubiquinol – the reduced and active form of coenzyme Q10 and a powerful antioxidant – significantly enhances mitochondrial function and reduces apoptosis in human donor corneal endothelial cells. However, ubiquinol is highly lipophilic, underscoring the need for an aqueous-based formulation of this mol. Herein, we report a highly dispersible and stable formulation comprising a complex of ubiquinol and gamma cyclodextrin (γ-CD) for use in aqueous-phase ophthalmic products. Docking studies showed that γ-CD has the strongest binding affinity with ubiquinol compared to α- or β-CD. Complexed ubiquinol showed significantly higher stability compared to free ubiquinol in different aqueous ophthalmic products including Optisol-GS corneal storage medium, balanced salt solution for intraocular irrigation, and topical Refresh artificial tear eye drops. Greater ROS scavenging activity was noted in a cell model with high basal metabolism and ROS generation (A549) and in HCEC-B4G12 human corneal endothelial cells after treatment with ubiquinol/γ-CD compared to free ubiquinol. Furthermore, complexed ubiquinol was more effective at lowering ROS, and at far lower concentrations, compared to free ubiquinol. Complexed ubiquinol inhibited lipid peroxidation and protected HCEC-B4G12 cells against erastin-induced ferroptosis. No evidence of cellular toxicity was detected in HCEC-B4G12 cells after treatment with complexed ubiquinol. Using a vertical diffusion system, a topically applied inclusion complex of γ-CD and a lipophilic dye (coumarin-6) demonstrated transcorneal penetrance in porcine corneas and the capacity for the γ-CD vehicle to deliver drug to the corneal endothelium. Using the same model, topically applied ubiquinol/γ-CD complex penetrated the entire thickness of human donor corneas with markedly greater ubiquinol retention in the endothelium compared to free ubiquinol. Lastly, the penetrance of ubiquinol/γ-CD complex was assayed using human donor corneas preserved for 7 days in Optisol-GS per standard industry practices, and demonstrated higher amounts of ubiquinol retained in the corneal endothelium compared to free ubiquinol. In summary, ubiquinol complexed with γ-CD is a highly stable composition that can be incorporated into a variety of aqueous-phase products for ophthalmic use including donor corneal storage media and topical eye drops to scavenge ROS and protect corneal endothelial cells against oxidative damage. This study involved multiple reactions and reactants, such as 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0Product Details of 38215-36-0).

3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0) belongs to thiazole derivatives. The thiazole ring has been identified as a central feature of numerous natural products, perhaps the most famous example of which is epothilone. 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.Product Details of 38215-36-0

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

Different effects of anti-VEGF drugs (Ranibizumab, Aflibercept, Conbercept) on autophagy and its effect on neovascularization in RF/6A cells was written by Wang, Yi;Yao, Yang;Li, Rong;Wu, Binghui;Lu, Huiqin;Cheng, Jing;Liu, Zhe;Du, Junhui. And the article was included in Microvascular Research in 2021.Category: thiazole The following contents are mentioned in the article:

Choroidal neovascularization (CNV) is the main pathol. change of wet age-related macular degeneration. Anti-VEGF drugs are the most commonly used treatment for CNV. The biggest drawback of anti-VEGF drugs is the recurrence of CNV, which requires repeated therapy several times. Autophagy activation may be involved in reducing the therapeutic effect of anti-VEGF drugs. So, this study aims to elucidate the effect and mechanism of anti-VEGF drugs on endothelial autophagy and neovascularization in vitro. RF/6A cells were randomly divided into five groups: The control group, hypoxia group (1% O2, 5% CO2, 94% N2), anti-VEGF group (group1: Ranibizumab 100 μg/mL; group2: Aflibercept, 400 μg/mL; group3: Conbercept, 100 μg/mL). Autophagy-related proteins were examined by Western blot. RFP-GFP-LC3 was used to detect autophagy and autophagic flow. Subsequently, we used autophagy inhibitors (3-MA or CQ) to inhibit Conbercept induced autophagy and to observe its effect on angiogenesis in vitro. Proliferation, migration, and tube formation of endothelial cells can be used to study neovascularization in vitro. In this research, the CCK-8 assay was used to detect cell proliferation. Cell migration and tube formation were assessed by wound assay and matrix method, resp. Flow cytometry and Tunel were used to detect cell apoptosis. Finally, the mechanism of Conbercept activated autophagy was studied. Western blot was used to detect the expression of p53 and DRAM (damage-regulated autophagy modulator), upstream activators of autophagy. The protein levels of Beclin-1 and LC3-2/1 in Ranibizumab and Conbercept groups were significantly higher than in the hypoxia group(P < 0.05). While the expression of P62 was decreased (P < 0.05). The autophagic flux was showed the same results. However, Aflibercept showed the opposite effect on autophagy. Compared with the Conbercept group, autophagy inhibitor 3-MA or CQ can further inhibit cell proliferation and promotes cell apoptosis (P < 0.05). Conbercept significantly inhibited cell migration compared with the hypoxia group (633.08 ± 72.52 vs. 546.33 ± 24.61), while the autophagy inhibitor group (3-MA or CQ) had a more obvious inhibition effect (309.75 ± 86.36 and 263.33 ± 68.67) (P < 0.05). For tube formation, the number of tube formation was decreased significantly in the Conbercept group (32.00 ± 2.00) compared to the hypoxia group (39.00 ± 1.53) and even further reduced in 3-MA or CQ group (24.00 ± 3.61, 20.00 ± 2.65). The length of master segments in the hypoxia group was 15,668.00 ± 894.11. It was decreased in Conbercept (13,885.34 ± 730.03). In 3-MA or CQ group, the length of master segments dropped further (11,997.00 ± 433.66, 10,617.67 ± 543.21). Compare with the hypoxia group, the expression P53 and DRAM were increased in the Conbercept group (P < 0.05). Autophagy-related proteins LC-3, Beclin-1, and DRAM were inhibited by P53 inhibitor Pifithrin-α (PFTα) (P < 0.05). Ranibizumab and Conbercept can trigger the autophagy of vascular endothelial cells while Aflibercept can inhibit it. The combination of Conbercept and autophagy inhibitor can significantly inhibit the formation of angiogenesis in vitro. The mechanism of autophagy activation is related to the activation of the p53/DRAM 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: 63208-82-2Category: thiazole).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles 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 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.Category: thiazole

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

Syntheses of heterocyclic compounds of nitrogen. CV. Benzothiazole derivatives. 9 was written by Takahashi, Torizo;Okada, Jutaro;Yamamoto, Yasuo. And the article was included in Yakugaku Zasshi in 1957.Category: thiazole The following contents are mentioned in the article:

A mixture of 12 g. 3-ClC₆H₄NH₂, 15 g. NH₄SCN, and 75 ml. AcOH at 5° treated dropwise with 16 g. Br in 32 g. AcOH, the product diluted with 4 volumes H₂O, neutralized with Na₂CO₃, the precipitate filtered off, taken up in 10% HCl, the HCl layer made alk. with NH₄OH, and the product recrystallized from C₆H₆ gave 6 g. 3,4-Cl(NCS)C₆H₃NH₂ (I), columns, m. 75°. Or, reducing 0.6 g. 3,4-Cl(NCS)C₆H₃NO₂ in 6 ml. concentrated HCl with 6 g. SnCl₂.2H₂O, suspending the precipitate in H₂O, alkalinizing with NaOH, and extracting with Et₂O gave C₆H₆-soluble I and C₆H₆-insoluble [2,4-Cl(H₂N)C₆H₃]₂S₂, m. 136-8°. 3-ClC₆H₄NHCSNH₂ (50 g.) in 150 ml. CHCl₃ treated dropwise with 44 g. Br in 30 ml. CHCl₃, heated 1 hr. on an H₂O bath, the solvent removed, the residue in 800 ml. H₂O and 5 ml. 48% HBr treated with a small amount of Na₂SO₃, made alk. with Na₂CO₃, and the precipitate recrystallized from dilute EtOH gave 28 g. 2-amino-5-chlorobenzothiazole (II), needles, m. 198°; the filtrate from II made alk. with K₂CO₃ and the precipitate recrystallized from dilute EtOH gave 16.5 g. 7-Cl analog (III) of II, needles, m. 145-50°. Or, the reduction of 0.6 g. 5,2-Cl(NCS)C₆H₃NO₂ with 6 g. SnCl₂.2H₂O gave 0.4 g. II, m. 196-8°. A mixture of 1 mole RC₆H₃.S.C(NH₂):N [R = 6-MeO (IIIA), 6-EtO (IV), 6-BuO (V), 4-Cl (VI), 5-Cl (VII), or 6-Cl (VIII)] (2 moles used in the case of III) in CHCl₃, 1 mole C₅H₅N (no addition in the case of III), and 1 mole 2-bromoacyl bromide or (ClCH₂CO)₂O heated 0.5-1 hr. on an H₂O bath, the solvent removed, and the product recrystallized from solvent gave RC₆CH₃.S.C(NHCOCHXR¹):N (IX) (R, R¹, X, and m.p. given): IIIA, H, Br, 164-5°; III, Me, Br, 148°; III, Et, Br, 123°; III, Me₂CH, Br, 128-8.5°; IV, H, Cl, 181°; IV, Me, Br, 145°; IV, Et, Br, 139°; IV, Me₂CH, Br, 115°; V, H, Br, 162-3°; V, Me, Br, 122°; V, Et, Br, 99-100°; V, Me₂CH, Br, 129°; VI, Me, Br, 152°; VII, H, Br, 178°; VII, Me, Br, 160°; VII, Et, Br, 182-3°; VII, Me₂CH, Br, 156-7°; VIII, H, Cl, 218°; VIII, Me, Br, 149°; VIII, Et, Br, 146°; VIII, Me₂CH, Br, 150°. A mixture of 1 mole IX and a C₆H₆ solution containing more than 2 moles Me₂NH in a sealed tube heated 1 hr. at 100°, kept overnight, and the solvent removed gave RC₆H₃.S.C(NHCOCHR¹NMe₂):N (X) (R, R¹, and m.p. given): III, H, 113-14°; III, Me, 113°; IV, H, 126° (as HCl salt); IV, Me, 178° (picrate); IV, Et, 91°; V, H, 96-7°; V, Me, 76-7°; VI, Me, 106-7°; VII, H, 144-5°; VII, Me, 163-4°; VII, Et, 120-1°; VIII, H, 136°; VIII, Me, 255° (decomposition) (as HCl salt); VIII, Et, 260° (decomposition) (as HCl salt). This study involved multiple reactions and reactants, such as 6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7Category: thiazole).

6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7) belongs to thiazole derivatives. Thiazoles are a class of five-membered rings containing nitrogen and sulfur with excellent antitumor, antiviral and antibiotic activities. 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.Category: thiazole

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

Antituberculous compounds. V. 2-Sulfanilamido-5-alkyl-1,3,4-oxadiazoles and -thiadiazoles and related isothiosemicarbazones and isothioureas was written by Brooks, J. D.;Charlton, P. T.;Macey, P. E.;Peak, D. A.;Short, W. F.. And the article was included in Journal of the Chemical Society in 1950.Application In Synthesis of 6-Butoxybenzo[d]thiazol-2-amine The following contents are mentioned in the article:

This work arose out of the observation that 2-sulfanilamido-5-methyl-1,3,4-oxadiazole (I), although virtually inactive against organisms normally sensitive to sulfonamides, exhibited a highly sp. activity in vitro against Mycobacterium tuberculosis. N⁴-Acyl derivatives of I were prepared from the acid anhydride in C₆H₆ (hexanoyl, m. 203°) or with the acid chloride in C₅H₅N (dodecanoyl, m. 124°; stearoyl, m. 128-9°). I(2.5g.)in 15 cc. H₂O and 4cc. concentrated HCl, treated with 3.3 g. iodine monochloride in 3 cc. concentrated HCl, gives 3 g. 2-(3,5-diiodosulfanilamido)-5-methyl-1,3,4-oxadiazole, m. 228-9°. 1-Acylthiosemicarbazones were prepared with the appropriate acid anhydride at 80° and finally at 110-20°; 10 g. of the crude product and 3 mols. PbO, heated 15-30 hrs. in 150-200 cc. EtOH, give the 5-alkyl derivatives of 2-amino-1,3,4-oxadiazole: 5-Am, m. 151° (N-sulfanilyl derivative, m. 148-9°; N⁴-Ac derivative, m. 186°); 5-hendecyl, m. 150-1° (N-sulfanilyl derivative, m. 105-7°); 5-heptadecyl, m. 143° (N-sulfanilyl derivative, m. 91-3°). 2-(p-Tolylsulfonamido)-5-methyl-1,3,4-oxadiazole, m. 152°. 1-Hexanoylthiosemicarbazide (22 g.) and 30 g. PhSO₃H, heated 15 min. on the steam bath and the aqueous solution basified with NH₄OH, give 17 g. 2-amino-5-amyl-1,3,4-thiadiazole, m. 195°; 2-sulfanilamido analog, m. 182° (N⁴-Ac derivative, m. 201-2°). In view of the unfavorable in vivo properties of the above compounds, a series of 3-alkylisothiosemicarbazones (II) and 2-alkylisothioureas was prepared p-BuOC₆H₄NCS (III) (4.25 g.) in 6 cc. absolute EtOH, treated with 1.2 cc. 90% N₂H₄.H₂O in 1 cc. EtOH and the crude product refluxed 3 hrs. with 2.2 g. BzH in 60 cc. EtOH, gives 4.5 g. benzaldehyde 4-p-butoxyphenylthiosemicarbazone, pale yellow, m. 164-5°. The II were prepared from the corresponding thiosemicarbazones by alkylation with EtONa and the appropriate alkyl halide in EtOH. Acetone 3-ethylisothiosemicarbazone (IV) HCl salt m. 153-4°; 3.2 g. IV and 2.1 g. NaHCO₃ in 25 cc. 50% EtOH, treated with 5.13 g. p-AcNHC₆H₄SO₂Cl, give 0.67 g. of the 4-(N-acetylsulfanilyl) derivative (V), m. 183-4°; 0.17 g. V and 1 cc. 2.5 N NaOH, heated 1 hr. at 100°, give 0.14 g. of the 4-sulfanilyl derivative, m. 186-7°. Benzaldehyde 3-butylisothiosemicarbazone HCl salt, m. 185-6°; 3-octyl homolog HCl salt, m. 176°; 3-hexadecyl homolog HCl salt, m. 162-3°; 3-(2-diethylaminoethyl) analog di-HCl salt, m. 192°. Benzaldehyde 4-phenyl-3-ethylisothiosemicarbazone (VA), pale yellow m. 78°; the 3-(2-diethylaminoethyl) analog forms a reineckate, m., 166-7° (decomposition). 4-(p-Butoxyphenyl) analog of VA, m. 90°. p-1-Pyrrolidylbenzaldehyde 3-ethylisothiosemicarbazone HCl salt, reddish brown, m. 245° (decomposition). p-Dimethylaminobenzaldehyde 3-ethylisothiosemicarbazone di-HCl salt, yellow, m. 219-20° (decomposition); boiling EtOH gives the mono-HCl salt, red, m. 230-2°. 2-Nitrobenzaldehyde analog HCl salt m. 169.5-70.5°. The S-alkylisothioureas were prepared from the appropriate thiourea and alkyl halides in boiling EtOH: N-phenyl-S-ethyl (VI) (picrate, yellow, m. 199.5°); S-Bu homolog (picrate, yellow, m. 144°); S-octyl homolog (picrate, yellow, m. 130.5°). N-p-Butoxyphenyl analog of VI (picrate, yellow, m. 162-3°); S-Bu homolog, (HI salt, m. 109-10°); S-octyl homolog (HBr salt, m. 96-6.5°). The activities of the thiadiazoles and the thiosemicarbazones are entirely unrelated. The low activity of the S-alkylisothioureas in the serum precluded in vivo activity. 2-Mercaptobenzimidazole and EtI, refluxed 2 hrs. in EtOH, give the 2-ethylmercapto analog m. 173.5-4.5°. p-BuOC₆H₄NH₂ (8.25 g.) and 9.5 g. NH₄NCS in 50 cc. 95% AcOH, treated with 10 g. Br in 13 cc. AcOH and kept overnight, give 2.2 g. 2-amino-6-butoxybenzothiazole, m. 119°. 2-Chloro-6-nitrobenzothiazole (10 g.) in 250 cc. BuOH, refluxed 20 hrs. with 1.07 g. Na in 50 cc. BuOH, give 4.15 g. 6-nitro-2-butoxybenzothiazole (VII), m. 60°; 10 g. VII, added in portions to 32 g. SnCl₂.₂H₂O in 40 cc. concentrated HCl at 70-80° and finally refluxed 30 min., gives 2.5 g. x-chloro-6-amino-2-butoxybenzothiazole-2HCl, m. 268° (decomposition). In the preparation of 2-mercapto-4-phenyl-6-methylpyrimidine (VIII), the fraction insoluble in EtOH, dilute HCl, or NaOH is bis(4-phenyl-6-methyl-2-pyrimidyl) disulfide, yellow, m. 185.5-6°; it results on oxidation of VIII in dilute NaOH with aqueous iodine. The appropriate S-alkylisothiourea-HX in 1 equivalent 2.5 N NaOH, treated with 1 mol. crude Et sodioformylpropionate, gives a 4-hydroxy-2-alkylmercapto-5-methylpyrimidine; with PCl₅ and POCl₃ (refluxed 45 min.) they give the 4-Cl compounds; these give the 4-NH₂ compounds when heated 6-8 hrs. with 8-10 parts (by weight) 10% EtOH-NH₃ at 135-50°. The following pyrimidines are reported: 2-methylmercapto-4-phenyl-6-methyl, b₁ 154-60°; 4-hydroxy-2-butylmercapto-5-methyl, m. 105-6°; 2-octylmercapto analog, m. 88-9°; 4-chloro-2-methylmercapto-6-methyl, b₁₅ 132°, m. 20-3°; 4-chloro-2-butylmercapto-5-methyl, b₁ 124-6°; octylmercapto homolog, b₂ 144-8°; 4-amino-2-methylmercapto-5-methyl, m. 130-1°; butylmercapto homolog, m. 85-6°; octylmercapto homolog, m. 85-6°. In no case were the compounds active at a dilution greater than 1:1000 in the presence of serum. This study involved multiple reactions and reactants, such as 6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7Application In Synthesis of 6-Butoxybenzo[d]thiazol-2-amine).

6-Butoxybenzo[d]thiazol-2-amine (cas: 14372-65-7) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1).Various laboratory methods exist for the organic synthesis of thiazoles. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.Application In Synthesis of 6-Butoxybenzo[d]thiazol-2-amine

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