2789-25-5

Usage

Uses

Used in Pharmaceutical Synthesis:
4-Amino-2-chloro-3-nitropyridine is used as a reagent for the synthesis of imidazopyridine-based fatty acid synthase inhibitors, which exhibit anti-HCV (hepatitis C virus) activity. These inhibitors target the essential enzymes involved in the replication and survival of the virus, offering a potential therapeutic approach for the treatment of hepatitis C.
Additionally, 4-Amino-2-chloro-3-nitropyridine is used as a reagent in the synthesis of acyclic nucleotides that are related to clitocine. These compounds have demonstrated antiviral activity, making them valuable candidates for the development of new antiviral drugs to combat various viral infections.
Used in Organic Chemistry Research:
Due to its reactive functional groups and the ability to undergo various chemical transformations, 4-Amino-2-chloro-3-nitropyridine is also utilized in organic chemistry research for the exploration of novel synthetic pathways and the development of new organic compounds with potential applications in various fields, such as materials science, agrochemistry, and medicinal chemistry.

Upstream product

• 14432-13-4 (2-chloro-pyridin-4-yl)-nitro-amine 
• 5470-18-8 2-Chloro-3-nitropyridine 
• 7664-93-9 sulfuric acid 
• 14432-12-3 4-Amino-2-chloropyridine 
• 109-09-1 2-chloropyridine 
• 2402-95-1 2-chloropyridine-N-oxide 
• 14432-16-7 2-chloro-4-nitropyridine-N-oxide 
• 89282-12-2 2,4-dihydroxy-3-nitropyridine 
• 5975-12-2 2,4-dichloro-3-nitro-pyridine 

Downstream Products

• 39217-08-8 2-chloropyridine-3,4-diamine 
• 24501-21-1 2,4-diamino-3-nitropyridine 
• 121370-68-1 tert-butyl 4-(1H-imidazo[4,5-c]pyridin-4-yl)piperazine-1-carboxylate 
• 6811-77-4 4-amino-1H-imidazo[4,5-b]pyrimidine 
• 881844-11-7 4-chloro-1-(p-methoxybenzyl)-1H-imidazo[4,5-c]pyridine 

Relevant academic research and scientific papers

Imidazopyridine-Based 5-HT6Receptor Neutral Antagonists: Impact of N1-Benzyl and N1-Phenylsulfonyl Fragments on Different Receptor Conformational States

G-protein coupled receptors (GPCRs) exist in an equilibrium of multiple conformational states, including different active states, which depend on the nature of the bound ligand. In consequence, different conformational states can initiate specific signal transduction pathways. The study identified compound 7e, which acts as a potent 5-hydroxytryptamine type 6 receptor (5-HT6R) neutral antagonist at Gs and does not impact neurite growth (process controlled by Cdk5). MD simulations highlighted receptor conformational changes for 7e and inverse agonist PZ-1444. In cell-based assays, neutral antagonists of the 5-HT6R (7e and CPPQ), but not inverse agonists (SB-258585, intepirdine, PZ-1444), displayed glioprotective properties against 6-hydroxydopamine-induced and doxorubicin-induced cytotoxicity. These suggest that targeting the activated conformational state of the 5-HT6R with neutral antagonists implicates the protecting properties of astrocytes. Additionally, 7e prevented scopolamine-induced learning deficits in the novel object recognition test in rats. We propose 7e as a probe for further understanding of the functional outcomes of different states of the 5-HT6R.

Design, synthesis and biological evaluation of novel substituted purine isosters as EGFR kinase inhibitors, with promising pharmacokinetic profile and in vivo efficacy

Novel substituted purine isosters, were designed and synthesized as potential inhibitors of the Epidermal Growth Factor Receptor (EGFR). The compounds were rationally designed through bioisosteric replacement of the central quinazoline core of lapatinib, an approved drug that inhibits both EGFR and HER2, another important member of this family of receptors. The new target molecules were evaluated as inhibitors of receptor phosphorylation at the cellular level, for their direct inhibitory action on the intracellular receptor kinase domain and for their cytotoxicity against the non-small cell lung cancer cell line A549 and breast cancer HCC1954, cell lines which are associated with overexpression of EGFR and HER2, respectively. The most potent derivatives were further studied for their cellular uptake levels and in vivo pharmacokinetic properties. One compound (23)displayed a noteworthy pharmacokinetic profile, and higher intracellular accumulation in comparison to lapatinib in the A549 cells, possibly due to its higher lipophilicity. This lead compound (23)was assessed for its efficacy in an EGFR positive xenograft model, where it successfully inhibited tumor growth, with a similar efficacy with that of lapatinib and with minimal phenotypic toxicity.

Environmental protection preparation method of 4-amino-2-chloro-3-nitropyridine

The invention relates to an environmental protection preparation method of 4-amino-2-chloro-3-nitropyridine. The method uses 3-amino propionitrile and trichloronitroethylene for 1,4-Addition and cyclization reaction to obtain 4-amino--2, 2, 3-trichloro-3-nitro-1, 2, 3, 6-tetrahydropyridine, and eliminates hydrogen chloride with an acid binding agent to prepare the 4-amino-2-chloro-3-nitropyridine.The method has the advantages of good reaction selectivity, good target product yield, high purity, short process flow, safe and simple operation, mild conditions, no waste acid and wastewater, environmental protection and low cost, and is carried out by a one-pot method.

Structure-activity relationships in fungal nucleobases transporters as dissected by the inhibitory effects of novel purine analogues

We have previously rationally designed, synthesized and tested a number of 3-deazapurine analogues, which inhibit the ubiquitous fungal nucleobase transporter FcyB, through binding in its major substrate binding site, by specifically interacting with Asn163. Here, in an effort to further understand the molecular details of structure-activity relationships in all three major nucleobase transporters of fungi, we extend this study by designing, based on our previous experience, synthesizing and testing further 3-deazapurine analogues. We thus identify seven new compounds with relatively high affinity (19–106 μΜ) for the FcyB binding site. Importantly, four of these compounds can also efficiently inhibit AzgA, a structurally and evolutionary distinct, but functionally similar, purine transporter. Contrastingly, none of the new compounds tested had any effect on the transport activity of the uric acid-xanthine transporter UapA, albeit this being a structural homologue of AzgA. Besides the apparent importance for understanding how nucleobase transporter specificity is determined at the molecular level, our work might constitute a critical step in the design of novel purine-related antifungals.

Pharmaceutical composition for treating hyperplasia of mammary glands as well as preparation method and application of pharmaceutical composition

The invention belongs to the technical field of medicine and particularly relates to a pharmaceutical composition for treating hyperplasia of mammary glands. The pharmaceutical composition has the structure in a formula shown in the description. The invention also relates to a preparation method and an application of the pharmaceutical composition for treating hyperplasia of mammary glands. The medicine can relieve mammary tissue hyperplasia lesion, has significant treatment effects on patients suffering from hyperplasia of mammary glands and is stable in curative effect, high in cure rate andlow in recurrence rate.

Site-Selective Copper-Catalyzed Amination and Azidation of Arenes and Heteroarenes via Deprotonative Zincation

Arene amination is achieved by site-selective C-H zincation followed by copper-catalyzed coupling with O-benzoylhydroxylamines under mild conditions. Key to this success is ortho-zincation mediated by lithium amidodiethylzincate base that is effective for a wide range of arenes, including nonactivated arenes bearing simple functionalities such as fluoride, chloride, ester, amide, ether, nitrile, and trifluoromethyl groups as well as heteroarenes including indole, thiophene, pyridine, and isoquinoline. An analogous C-H azidation is also accomplished using azidoiodinane for direct introduction of a useful azide group onto a broad scope of arenes and heteroarenes. These new transformations offer rapid access to valuable and diverse chemical space of aminoarenes. Their broad applications in organic synthesis and drug discovery are demonstrated in the synthesis of novel analogues of natural product (-)-nicotine and antidepressant sertraline by late-stage amination and azidation reactions.

Design and synthesis of purine analogues as highly specific ligands for FcyB, a ubiquitous fungal nucleobase transporter

In the course of our study on fungal purine transporters, a number of new 3-deazapurine analogues have been rationally designed, based on the interaction of purine substrates with the Aspergillus nidulans FcyB carrier, and synthesized following an effective synthetic procedure. Certain derivatives have been found to specifically inhibit FcyB-mediated [3H]-adenine uptake. Molecular simulations have been performed, suggesting that all active compounds interact with FcyB through the formation of hydrogen bonds with Asn163, while the insertion of hydrophobic fragments at position 9 and N6 of 3-deazaadenine enhanced the inhibition.

4-amino-2-chloro-3-nitro pyridine synthesis method

The invention discloses a method for synthesizing 4-amino-2-chlorine-3-nitro pyridine. The method comprises the following steps: adopting 65% nitric acid and concentrated sulfuric acid as mixed acid for nitratlon reaction, wherein the yield of the prepared isomer 4-amino-chlorine-3-nitro pyridine and 4-amino-2-chlorine-5-nitro pyridine is 95 to 98%, the purity is 95 to 99.5%, and subsequently purifying through recrystallization, effectively separating the prepared 4-amino-2-chlorine-3-nitro pyridine and 4-amino-2-chlorine-5-nitro pyridine, wherein the yield of the prepared 4-amino-2-chlorine-3-nitro pyridine is 75 to 85%, the purity of the prepared 4-amino-2-chlorine-3-nitro pyridine is 95 to 99%, the yield of the prepared 4-amino-2-chlorine-5-nitro pyridine is 15 to 25%, and the purity of the prepared 4-amino-2-chlorine-5-nitro pyridine is 95 to 99%. The method is applicable to preparation of 4-amino-2-chlorine-3-nitro pyridine and 4-amino-2-chlorine-5-nitro pyridine, and medicines such as an E1 active enzyme inhibitor, an adenosine homocysteine hydrolase inhibitor, a PLK1 recombinant protein inhibitor and benzimidazole can be further prepared.

ANTI-FIBROTIC PYRIDINONES

This application relates to polycyclic compounds with a pyridinone or pyridinone derivative core including, substituted pyridinones, 5,6- and 6,6- bicyclic heterocycles and substituted pyridine-thiones. This application also discloses methods of preparing these polycyclic compounds, pharmaceutical compositions and medicaments comprising said compounds and methods to treat, prevent or diagnose diseases, disorders or conditions associated with fibrosis.

Structure-activity relationships in Toll-like receptor 7 agonistic 1H-imidazo[4,5-c]pyridines

Engagement of TLR7 in plasmacytoid dendritic cells leads to the induction of IFN-α/β which plays essential functions in the control of adaptive immunity. We had previously examined structure-activity relationships (SAR) in TLR7/8-agonistic imidazoquinolines with a focus on substituents at the N 1, C2, N3 and N4 positions, and we now report SAR on 1H-imidazo[4,5-c]pyridines. 1-Benzyl-2-butyl-1H-imidazo[4,5-c] pyridin-4-amine was found to be a pure TLR7-agonist with negligible activity on TLR8. Increase in potency was observed in N6-substituted analogues, especially in those compounds with electron-rich substituents. Direct aryl-aryl connections at C6 abrogated activity, but TLR7 agonism was reinstated in 6-benzyl and 6-phenethyl analogues. Consistent with the pure TLR7-agonistic behavior, prominent IFN-α induction in human PBMCs was observed with minimal proinflammatory cytokine induction. A benzologue of imidazoquinoline was also synthesized which showed substantial improvements in potency over the parent imidazopyridine. Distinct differences in N6-substituted analogues were observed with respect to IFN-α induction in human PBMCs on the one hand, and CD69 upregulation in lymphocytic subsets, on the other.