Day: November 7, 2022

On April 15, 2013, Wirasorn, Kosin; Ngamprasertchai, Thundon; Chindaprasirt, Jarin; Sookprasert, Aumkhae; Khantikaew, Narong; Pakkhem, Ake; Ungarereevittaya, Piti published an article.Name: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate The title of the article was Prognostic factors in resectable cholangiocarcinoma patients: Carcinoembryonic antigen, lymph node, surgical margin and chemotherapy.. And the article contained the following:

AIM: To evaluate outcomes in resectable cholangiocarcinoma patients and to determine prognostic factors. METHODS: A retrospective study was conducted among newly-diagnosed cholangiocarcinoma patients from January 2009 to December 2011 who underwent curative resection in Srinakarind Hospital (a 1000-bed university hospital). Two hundred and sixty-three cholangiocarcinoma patients with good performance were enrolled. These patients had pathological reports with clear margins or microscopic margins. Prognostic factors which included clinical factors, serum liver function test as well as serum tumor makers at presentation, tumor data, and receiving adjuvant chemotherapy were determined by uni- and multivariate analysis. RESULTS: The median overall survival time was 17 mo (95%CI: 13.2-20.7); and 1-, 2-, and 3- year survival rates were 65.5%, 45.2% and 35.4%. Serum albumin levels, serum carcinoembryonic antigen (CEA) levels, staging classifications by American Joint Committee on cancer, pathological tumor staging, lymph node metastases, tumor grading, surgical margin status, and if adjuvant chemotherapy was administered, were shown to be significant prognostic factors of resectable cholangiocarcinoma by univariate analysis. Multivariate analysis, however, established that only abnormal serum CEA [hazard ratio (HR) 1.68; P = 0.027] and lymph node metastases (HR 2.27; P = 0.007) were significantly associated with a decrease in overall survival, while adjuvant chemotherapy (HR 0.71; P = 0.067) and surgical margin negative (HR 0.72; P = 0.094) tended to improve survival time. CONCLUSION: Serum CEA and lymph node metastases which were associated with advanced stage tumors become strong negative prognostic factors in cholangiocarcinoma. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Name: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

The Article related to adjuvant, carcinoembryonic antigen, chemotherapy, cholangiocarcinoma, hepatectomy, lymph nodes, neoplasm metastasis, prognosis, surgical margin status, survival rate, and other aspects.Name: N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Bernstein, Jack; Stearns, Barbara; Shaw, Elliott; Lott, W. A. published an article in 1947, the title of the article was Derivatives of 2,6-diaminopyridine.Related Products of 51566-22-4 And the article contains the following content:

Since 2,6-diaminopyridine (I) showed an appreciable antiparasitic activity when tested against Plasmodium lophurae in ducklings, various derivatives of I have been prepared to determine if further substitution in the mol. would increase the antiparasitic activity of the parent compound I (66 g.) in 300 cc. dioxane, treated dropwise with 23.5 g. AcCl in 50 cc. dioxane (0.5 h.) at 25-30° and stirred 2 addnl. hrs., gives 40% of the 2-Ac derivative (II), m. 156-7°; 2-butyryl derivative m. 152-3°, 25%; 2-salicyloyl derivative (prepared from o-AcOC6H4COCl and purified by precipitation from dilute HCl with dilute NaOH) m. 178-9°, 44%; 2-[phenyl(acetoxy)acetyl] derivative (as HCl salt with 1 mol. H2O) m. 151-3°, 23%. N,N’-Bis(6-amino-2-pyridyl)adipamide m. 228-9°, 72%; N,N’-bis(6-amino-2-pyridyl)sebacamide m. 152-5°, 55%. 1,3-Bis(6-amino-2-pyridyl)urea does not melt, 71%. (CH2CO)2O (30 g.) in 200 cc. dioxane, treated slowly with 33 g. I in 200 cc. dioxane and heated 3 h. on the steam bath, gives 57% N-(6-amino-2-pyridyl)succinamic acid, m. 174-5° (decomposition). I (46 g.) and 222 cc. AcCH2CO2Et, heated 15 min. at 160° and the product in EtOH treated with alc. HCl, give 40% 2,6-bis(acetylacetamido)pyridine-HCl, m. 195-8°; the filtrate yields 10% of the 2-acetylacetamido derivative, m. 146-7°. I (22 g.) and 22.6 g. NCCH2CO2Et, heated 2 h. at 165°, give 85% 2-amino-6-cyanoacetamidopyridine, m. 152-3°. 2-Acetamido-6-carbethoxyacetamidopyridine m. 150-1.5°, 41%. I (282 g.) and 290 g. HOCH2CO2H, fused 15 h. at 120° under reduced pressure, give 35% 2,6-bis(glycolylamino)pyridine, m. 220-1°. I (33 g.) in 200 cc. absolute EtOH containing 6.9 g. Na and 43 g. Et2NCH2CO2Et, refluxed 2 h., give 55% 2,6-bis(diethylaminoacetamido)pyridine, m. 109.5-10.5°. I (22 g.) and 27 g. AcNHCOCl, ground in a mortar and 35 cc. C5H5N added, give 19% 2,6-bis(acetamidoacetamido)pyridine, m. 260-1°. MeC(:NH)NH2.HCl (24.6 g.) in 100 cc. absolute EtOH, added to 22 g. I in 150 cc. absolute EtOH, stirred 3 h., and allowed to stand overnight at room temperature, give 38% N-(6-amino-2-pyridyl)acetamidine-HCl, m. 246-7° (decomposition). I (396 g.) in 8 l. H2O, treated dropwise with 195 g. ClCO2Et (3 h.), gives 76% 2-amino-6-carbethoxyaminopyridine (III), m. 109-12°. I (33 g.) in 500 cc. H2O, 200 cc. N HCl, and 300 g. ice, treated dropwise with 33 g. ClCO2Et, stirred 2 h., 200 cc. N HCl added, and the mixture allowed to stand overnight at 10°, gives 55% 2,6-bis(carbethoxyamino)pyridine, m. 132.5-3.5°, and 12 g. III. III (21.6 g.) in 120 cc. 3 N EtOH-NH3, heated 12 h. at 110°, gives 75% 2-amino-6-ureidopyridine, m. 175-6° (decomposition). I (48 g.) and 48 g. CO(NH2)2, heated 36 h. at 130°, give 49% 2,6-diureidopyridine, does not melt below 300° (purified by extraction with 300 cc. 3% HCl and crystallization of the residue from H2O). I (12 g.) in 1500 cc. C6H6, treated dropwise with 17.9 g. p-EtOC6H4NCO in 75 cc. C6H6, gives 86% 2-(p-ethoxyphenylureido)-6-aminopyridine, m. 168-9°; 2-(2-nitro-4-methoxyphenylureido)-6-aminopyridine m. 208-10°, 73%; reduction over Pt oxide gives 50% of the corresponding 2-(2-amino-4-methylphenylureido) derivative, m. 182-4°. I (154 g.) and 200 g. of the HCl salt of I, heated 12 h. at 190°, give 60% bis(6-amino-2-pyridyl)amine, m. 172-3° (the HCl salt does not melt). 2,6-Dibromopyridine (IV) (38 g.) and 160 cc. 25% aqueous MeNH2, heated 8 h. at 190°, give 59% 2,6-bis(methylamino)pyridine, m. 70-1°; this results in 20% yield from 27.6 g. 2-amino-6-bromopyridine (V) and 110 cc. 25% aqueous MeNH2 on heating 30 h. at 190°. V (80 g.) and 200 cc. EtNH2, heated 36 h. at 170-80°, give 81% 2-amino-6-(diethylamino)pyridine (VI), b4.5 122-3°, m. 34-5° (HCl salt, m. 143-4°). IV (45 g.) and 27.8 g. Et2NH in 100 cc. absolute EtOH, heated 8 h. at 170-80°, give 85% 2-bromo-6-(diethylamino)pyridine (VII), b4 97-9°; VII does not react with NH4OH (d. 0.9) at 170-80° (8 h.); 11 g. VII and 35 cc. 5 N EtOH-NH3, heated 25 h. at 170°, also did not react; 18.8 g. VII in 100 cc. NH4OH (d. 0.9) containing 1 g. CuSO4.5H2O, heated 30 h. at 140-5°, gives 44% VI. IV (35.6 g.) and 100 cc. Et2NH containing 4 cc. 25% CuSO4.5H2O, heated 30 h. at 160°, give 76% 2,6-bis(diethylamino)pyridine, b3 120-2° (HCl salt, m. 120-2°). 2-Amino-6-(3-diethylaminopropylamino)pyridine-HCl m. 65-75°, 53%; 2-acetamido-6-(4-diethylamino-1-methylbutylamino)pyridine m. 106-8° (51%). 2-Acetamido-6-(3-keto-1-methylbutylideneamino)-pyridine, 2,6-AcNHC5H3N(N:CMeCH2Ac), m. 146-7.5°, 40%. 2-Acetamido-6-(2,5-dimethyl-1-pyrryl)pyridine m. 147.5-8.5°, 54%. 2-Methoxy-6,9-dichloroacridine (11.2 g.) in 50 g. PhOH, warmed on the steam bath, treated with 11 g. I, and heated 3 h., gives 61% 2-methoxy-6-chloro-9-(6-amino-2-pyridylamino)acridine, yellow, m. 232-3°. II (30.2 g.), added in small portions to 100 cc. HNO3 (d. 1.5) at -5° to -2° and stirred an addnl. 30 min., gives 65% of the Ac derivative, decompose violently at 193°, of 2-nitramino-6-aminopyridine (VIII), darkens at 240-50° (hydrolysis by refluxing 1 h. with N NaOH); reduction of 15.4 g. VIII in 300 cc. 10% NaOH at 0-2° with 31 g. Zn gives 69% 2-hydrazino-6-aminopyridine, pale yellow, m. 93-4°; warmed 2 h. on the steam bath with AcCH2CO2Et (N atm.), there results 44% 1- (6-amino-2-pyridyl)-3-methyl-5-pyrazolone, m. 188-9.5°. 3-Methylpyridine (80 g.), 160 g. PhNMe2, and 144 g. NaNH2, heated 10 h. at 130-50° and 6 h. at 170-200°, give 4% 2,6-diamino-3-methylpyridine, m. 149-50°. 2,6-Dihydroxy-4-methylpyridine (9 g.) and 30 g. PBr3, heated 4.5 h. at 180°, give 36% 2,6-dibromo-4-methylpyridine, m. 74-5°; heated with NH4OH (d. 0.9) 27 h. at 195°, there results 71% 2,6-diamino-4-methylpyridine, m. 87-8°, which on sublimation m. 109-11° but reverts to the lower m.p. on standing. 2,6-Diamino-3-iodopyridine (23.5 g.) in 25 cc. AcOH and 35 cc. Ac2O, heated 1 h. on the steam bath, gives 33% of the di-Ac derivative, m. 210-11°. I (38 g.) in 550 cc. H2O, treated with 93 g. iodine and 93 g. KI in 150 cc. H2O, the mixture stirred 8 h., and allowed to stand overnight at room temperature, gives 36% 2,6-diamino-3,5-diiodopyridine-HCl, m. 160-5°; the free base m. 209-10°. 3-Methoxypyridine (IX) (15.8 g.) in 100 cc. concentrated H2SO4, treated dropwise (with cooling) with 25 cc. HNO3 (d. 1.6) and warmed 6 h. on the steam bath, gives 12.2 g. 3-methoxy-2,6-dinitropyridine (X), m. 114-15°. IX (57 g.), added to 130 cc. concentrated H2SO4 at 5°, the mixture treated with 70 cc. HNO3 (d. 1.6), and heated 1 h. on the steam bath, yields 38 g. 2-nitro-3-methoxypyridine (XI), m. 73-5°; 5 g. XI in 15 cc. concentrated H2SO4, treated with 4 cc. HNO3 (d. 1.6), gives 4.4 g. X. Catalytic reduction (Pt oxide) of 16.8 g. X in 500 cc. AcOH and 250 cc. Ac2O at room temperature (4 h.) gives 60% 3-methoxy-2,6-diacetamidopyridine, m. 173.5-4.5°. 2,3,6-Triaminopyridine-2HCl in 200 cc. H2O and 25 g. Ac2 in 200 cc. H2O, boiled 4 min., yield 98% 2,3-dimethyl-6-aminopyrido[2,3]pyrazine, m. 227-8°; 6-aminopyrido[2,3]pyrazine m. 267°, 62%. 2,3,6-Triaminopyridine oxalate (80 g.) in 150 cc. (CO2Et)2, heated 90 min. at 185°, gives 68% 2,3-dihydroxy-6-aminopyrido[2,3]pyrazine, does not m. below 300°. Addition of 23.8 g. 2,6-diacetamido-3-nitropyridine to 100 g. SnCl2.2H2O in 150 cc. concentrated HCl gives 26% 2-methyl-5-amino-1-imidazo[b]pyridine-HCl; neither the base nor the salt melts. I (55 g.) and 194 g. KCNS in 1 l. 95% AcOH, treated dropwise at -5° to -10° with 26 cc. Br, give 24% 2,5-diaminopyrido[2,3-d]thiazole (XII), m. 138-9°; II likewise gives the 5-Ac derivative of XII, m. 184-5°. I (66 g.) in 2 l. AcOH, treated with 460 g. KCNS in 100 cc. H2O and then at 0-3° with 64 cc. Br, with stirring 1 h. at room temperature, yields 22% 2,6-diaminopyrido[2,3-d,6,5-d’]bisthiazole, does not melt below 300°. I (25 g.), 29 g. I.HCl, and 42 g. benzoin, heated 1 h. at 185°, yield 89% 2,3-diphenyl-6-amino-1-pyrrolo[2,3-b]pyridine, m. 234.5-5.5°. 2-Amino-6-(3-keto-1-methylbutylideneamino)pyridine (16 g.) in 100 cc. 85% H3PO4, warmed 1 h. on the steam bath, gives 84% 2,4-dimethyl-7-amino-1,8-naphthyridine, m. 216-18°; this results in 85% yield from 5 g. I and 5 cc. CH2Ac2 in 25 cc. 85% H3PO4 on warming 30 min. on the steam bath. 2,7-Dihydrazino-4-methyl-1,8-naphthyridine-2HCl-2H2O (23 g.) and 18 g. AcCH2CO2Et in 200 cc. 50% EtOH, heated 5 min. at 70°, give 84% 2,7-bis(3-methyl-5-keto-1-pyrazolyl)-4-methyl-1,8-naphthyridine, m. 260-2°. The most active of these compounds (II, XII, and the di-Ac derivative of I) are only 1/3 as active as quinine as antiparasitic agents for Plasmodium lophurae in ducklings. The experimental process involved the reaction of 3-Methylpyridine-2,6-diamine(cas: 51566-22-4).Related Products of 51566-22-4

The Article related to aminopyridines, malaria and other aspects.Related Products of 51566-22-4

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On December 16, 1971, Nicolson, Adrian published a patent.Application of 34968-33-7 The title of the patent was Chlorofluoropyridines. And the patent contained the following:

The title compounds were prepared by fluorination of chloropyridines with KF or NaF in a nonhydroxylic solvent, e.g. tetramethylene sulfone (I) or AcNMe2, in the presence of alcs., acids, or bases, e.g. MeOH, HO(CH2)2OH, glycerol, EtCO2H, or Bu3N. Thus, pentachloropyridine was added to KF (1:5.7 mole %) in I. ClCH2CO2H was added and the mixture refluxed 2 hr to give 79% fluorinated pyridines consisting of 3,5-dichlorotrifluoropyridine 97.5, pentafluoropyridine+3-chlorotetrafluoropyridine 2.2, and 3,5,6-tri-chlorodifluoropyridine 0.4%. Similarly prepared were 4-chloro-2-fluoro-, 2-chloro-4-fluoro-, 2,4-difluoro-, 6-chloro-2,4-difluoro,-and 4-chloro-2,6-difluoropyridine. The experimental process involved the reaction of 4-Chloro-2,6-difluoropyridine(cas: 34968-33-7).Application of 34968-33-7

The Article related to chlorofluoropyridine preparation, fluorochloropyridine preparation, pyridine chlorofluoro preparation, fluorination and other aspects.Application of 34968-33-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Sicho, Vladislav; Kralova, Blanka published an article in 1966, the title of the article was Influence of antivitamins on the microbiological biosynthesis of vitamins. II. Stimulation of nicotinic acid biosynthesis in the microorganism Saccharomyces cerevisiae by pyridine-3-sulfonic acid.Formula: C5H5NO3S And the article contains the following content:

The influence of the antivitamin of nicotinic acid (I), pyridine-3-sulfonic acid (II) on I biosynthesis in S. cerevisiae was investigated. II stimulated I synthesis 3-fold when added at 25 μg./100 g. nutrient media. The increased production of I probably results from the compensating response of the respective controlling systems to the competitive inhibition of the antivitamin. The experimental process involved the reaction of Pyridine-3-sulfonic acid(cas: 636-73-7).Formula: C5H5NO3S

The Article related to saccharomyces nicotinic acid, nicotinic acid saccharomyces, pyridinesulfonate nicotinate yeast, yeast pyridinesulfonate nicotinate, antivitamin yeast nicotinate, saccharomyces and other aspects.Formula: C5H5NO3S

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Grossowicz, N.; Halpern, Y. S. published an article in 1956, the title of the article was Inhibition of nicotinamidase activity in cell-free extracts of Mycobacterium phlei by 3-acetylpyridine.Application In Synthesis of Pyridine-3-sulfonic acid And the article contains the following content:

Nicotinic acid, α-picolinic acid, trigonelline, 6-aminonicotinamide, isonicotinoyl hydrazide, pyridine-3-sulfonic acid, and 3-acetylpyridine were tested as inhibitors of nicotinamidase activity in M. phlei, by employing cell-free extracts Only the last was strongly inhibitory. The inhibition was of the competitive type. The experimental process involved the reaction of Pyridine-3-sulfonic acid(cas: 636-73-7).Application In Synthesis of Pyridine-3-sulfonic acid

The Article related to mycobacterium, nicotinic acid/derivatives, pyridines/effects, mycobacterium phlei and other aspects.Application In Synthesis of Pyridine-3-sulfonic acid

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Levinson, H. Z.; Barelkovsky, J.; Bar Ilan, A. R. published an article in 1967, the title of the article was Nutritional effects of vitamin omission and anti-vitamin administration on development and longevity of the hide beetle Dermestes maculatus.Reference of Pyridine-3-sulfonic acid And the article contains the following content:

The development of newly hatched larvae to adulthood on semisynthetic diets requires most members of the B-vitamin group. Mortality and cannibalism is increased and pupation is decreased in the absence of nicotinic acid, pantothenic acid, biotin, pyridoxine, folic acid, or all the B-vitamins, while omission of riboflavine or thiamine from the diet permits partial or almost complete development into beetles but only after prolonged periods. There is no specific requirement for inositol. Vitamin antagonists such as 4-deoxypyridoxine, pyridine-3-sulfonic acid, and D-pantothenol, but not pantoyltaurine, prolong all stages of the life period. Neopyrithiamine, on the other hand, strongly reduces the larval period and prevents development. It is probable that the continuous administration of antimetabolites, such as the antivitamins, may have ecological implications on the size of the insect population through a reduction of the annual generation number The experimental process involved the reaction of Pyridine-3-sulfonic acid(cas: 636-73-7).Reference of Pyridine-3-sulfonic acid

The Article related to insect vitamin nutrition, antivitamins insect, antimetabolites insect, neopyrithiamine insect, vitamin insect nutrition, nutrition insect vitamin, avidins role: anst (analytical study), dermestes, vitamins and other aspects.Reference of Pyridine-3-sulfonic acid

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Dubash, Pesi J.; Rege, Dinanath V. published an article in 1968, the title of the article was Chlorophyll formation in Euglena gracilis var bacillaris. Interference by vitamin analogs.HPLC of Formula: 636-73-7 And the article contains the following content:

The relations between vitamins and chlorophyll synthesis in non-proliferating E. gracilis var bacillaris cells were studied. Although vitamin B12 deficiency increased cell size and cell mass in light-grown Euglena, it did not significantly affect chlorophyll synthesis. Furthermore, inhibition of chlorophyll synthesis by 2,6-diaminopurine, an antimetabolite of vitamin B12, was not abolished by vitamin B12. Other vitamin B12 antimetabolites, such as 6-mercaptopurine, sulfanilamide, and benzimidazole, did not inhibit pigment synthesis. Inhibition of chlorophyll synthesis by isoniazid (2000 μg./ml.) was not relieved by niacin (200 μg./ml.). In fact, niacin itself inhibited both growth and pigment synthesis. However, inhibition by niacin was prevented by pyridine-3-sulfonate (200 g./ml.). Niacin and its analogs, isoniazid and niacinamide, were also more inhibitory to growth in the dark than in the light. Inhibition of growth by niacin in the light was relieved by 1% glucose or pyruvate and by a large concentration (5000 μμg./ml.) of vitamin B12. Aminopterin, deoxypryridoxine, and 2-chloro-p-aminobenzoic acid did not affect chlorophyll synthesis in nonproliferating Euglena. However, 2-chloro-p-aminobenzoic acid (25 μg./ml.) inhibited growth 63.8% in the dark and 54.0% in the light. Thiamine deficiency inhibited growth, and such suboptimally grown Euglena also synthesized less chlorophyll during subsequent illumination under non-proliferation conditions. The neg. growth response of light-grown Euglena to niacin up to concentrations of 70 μg./ml. suggested that this organism could be used for the bioassay of niacin. The 50% growth inhibition level for niacin in the light was 46 μg./ml. 23 references. The experimental process involved the reaction of Pyridine-3-sulfonic acid(cas: 636-73-7).HPLC of Formula: 636-73-7

The Article related to chlorophyll formation euglena, vitamin interference chlorophyll, euglena formation chlorophyll, chlorophylls role: biol (biological study), euglena, vitamins and other aspects.HPLC of Formula: 636-73-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Gaut, Z. N.; Solomon, H. M. published an article in 1971, the title of the article was Inhibition of nicotinate phosphoribosyltransferase in human platelet lysate by nicotinic acid analogs.Application In Synthesis of Pyridine-3-sulfonic acid And the article contains the following content:

Nicotinate phosphoribosyltransferase in human platelet lysate has an apparent Km of 24 μM, is Mg2+-dependent, and catalyzes the first step in NAD biosynthesis (substrate: nicotinic acid). The pyridine N and carboxyl groups are important for interaction with the enzyme; large substituents (Br, NH2, CH2OH) in the 2-position of nicotinic acid apparently create steric hindrance of the pyridine N and produce low inhibitory activity for these compounds toward the enzyme. Positions 4 and 5 are also involved sterically since compounds such as 4-hydroxynicotinic acid are not inhibitory (at 0.5mM). The data indicate a size-restricted, hydrophobic region at the enzyme active site to accommodate atoms 4, 5, and possibly 6 of the pyridine ring. The experimental process involved the reaction of Pyridine-3-sulfonic acid(cas: 636-73-7).Application In Synthesis of Pyridine-3-sulfonic acid

The Article related to nicotine phosphoribosyltransferase inhibition, active site nicotine phosphoribosyltransferase, transferase nicotine phosphoribosyl inhibition, blood platelet, michaelis constant, reaction kinetics, structure-activity relationship and other aspects.Application In Synthesis of Pyridine-3-sulfonic acid

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Molina, Jean A. E.; Alexander, Martin published an article in 1967, the title of the article was The effect of antimetabolites on nodulation and growth of leguminous plants.COA of Formula: C5H5NO3S And the article contains the following content:

The influence of antimetabolites of amino acids, vitamins, auxins, purines, and pyrimidines on nodule formation and growth of legumes was investigated using Lotus corniculatus and excised roots of Phaseolus vulgaris. Many of the antimetabolites were toxic to L. corniculatus plants, P. vulgaris roots, or both at the concentrations tested, but several increased top length without affecting root development of the former species. Nodule abundance on L. corniculatus was increased by indole, 2-phenylbutyric acid, D- and L-leucine, barbituric acid, oxythiamine, and quercetin. α-Picolinic acid, a niacin antagonist, prevented nodule formation by this plant species, although it had no apparent effect on root or top growth or on proliferation of the infective rhizobium in vitro. No such influence on nodulation of L. corniculatus was noted with pyridine-3-sulfonate, another niacin antimetabolite. Benzene hexachloride and α-methylglutamic acid inhibited nodulation without seemingly affecting development of excised bean roots, while pyridine-3-sulfonate markedly enhanced nodulation. Nodulation of excised roots of Medicago saliva and Melilotus alba inoculated with infective rhizobia was demonstrated. 17 references. The experimental process involved the reaction of Pyridine-3-sulfonic acid(cas: 636-73-7).COA of Formula: C5H5NO3S

The Article related to nodulation legumes, niacin legumes nodules, legumes nodulation, indoles legumes nodules, phenylbutyrate legumes nodules, antimetabolites legumes nodules, alfalfa, amino acids, bean, hormones, plant, lotus (genus), medicago sativa, melilotus, phaseolus vulgaris, root nodule, sweet clover, vitamins and other aspects.COA of Formula: C5H5NO3S

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

On December 31, 2018, Wang, Bingbing; Parobchak, Nataliya; Martin, Adriana; Rosen, Max; Yu, Lumeng Jenny; Nguyen, Mary; Gololobova, Kseniya; Rosen, Todd published an article.Quality Control of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate The title of the article was Screening a small molecule library to identify inhibitors of NF-kappaB inducing kinase and pro-labor genes in human placenta. And the article contained the following:

The non-canonical NF-kappaB signaling (RelB/p52) pathway drives pro-labor genes in the human placenta, including corticotropin-releasing hormone (CRH) and cyclooxygenase-2 (COX-2), making this a potential therapeutic target to delay onset of labor. Here we sought to identify small mol. compounds from a pre-existing chem. library of orally active drugs that can inhibit this NF-kappaB signaling, and in turn, human placental CRH and COX-2 production We used a cell-based assay coupled with a dual-luciferase reporter system to perform an in vitro screening of a small mol. library of 1,120 compounds for inhibition of the non-canonical NF-kappaB pathway. Cell toxicity studies and drug efflux transport MRP1 assays were used to further characterize the lead compounds We have found that 14 drugs have selective inhibitory activity against lymphotoxin beta complex-induced activation of RelB/p52 in HEK293T cells, several of which also inhibited expression of CRH and COX-2 in human term trophoblast. We identified sulfapyridine and propranolol with activity against CRH and COX-2 that deserve further study. These drugs could serve as the basis for development of orally active drugs to affect length of gestation, first in an animal model, and then in clin. trials to prevent preterm birth during human pregnancy. The experimental process involved the reaction of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate(cas: 132-20-7).Quality Control of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

The Article related to placenta nf kappa b small mol, Pharmacology: Methods and other aspects.Quality Control of N,N-Dimethyl-3-phenyl-3-(pyridin-2-yl)propan-1-amine maleate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem