51935-42-3

Basic information

• Product Name: AKOS BBS-00002548
• Synonyms: AKOS BBS-00002548;AURORA KA-6764;CHEMBRDG-BB 4004788;1-CHLORO-4-HYDRAZINOPHTHALAZINE;4-CHLORO-1-HYDRAZINOPHTHALAZINE;1-chloro-4-hydrazinyl-Phthalazine;1-(4-chlorophthalazin-1-yl)hydrazine;1-chloro-4-hydrazineylphthalazine
• CAS NO: 51935-42-3
• Molecular Formula: C₈H₇ClN₄
• Molecular Weight: 194.62
• Mol File: 51935-42-3.mol
• Article Data: 10

Chemical Properties

• Boiling Point: 517.8 °C at 760 mmHg
• Flash Point: 267 °C
• Appearance: /
• Density: 1.513 g/cm³
• Vapor Pressure: 7.93E-11mmHg at 25°C
• Refractive Index: 1.774
• Storage Temp.: under inert gas (nitrogen or Argon) at 2–8 °C
• Solubility: DMSO, Methanol:Water
• CAS DataBase Reference: AKOS BBS-00002548(CAS DataBase Reference)
• NIST Chemistry Reference: AKOS BBS-00002548(51935-42-3)
• EPA Substance Registry System: AKOS BBS-00002548(51935-42-3)

Safety Data

• Hazardous Substances Data: 51935-42-3(Hazardous Substances Data)

Usage

Uses

4-Chloro-1-hydrazinophthalazine is an intermediate in the synthesis of novel 1,2,4-triazolo[3,4-a]phthalazine derivatives with anticancer activities.

InChI:InChI=1/C8H7ClN4/c9-7-5-3-1-2-4-6(5)8(11-10)13-12-7/h1-4H,10H2,(H,11,13)

Upstream product

• 85-44-9 phthalic anhydride 

Downstream Products

• 484-23-1 1,4-bis(hydrazino)phthalazine 
• 87539-80-8 Acetic acid 4-(6-chloro-[1,2,4]triazolo[3,4-a]phthalazin-3-yl)-phenyl ester 
• 87539-60-4 N-(4-Chloro-phthalazin-1-yl)-N'-[1-(2,4,5-trimethoxy-phenyl)-meth-(E)-ylidene]-hydrazine 
• 87539-60-4 N-[4-Chloro-2H-phthalazin-(1Z)-ylidene]-N'-[1-(2,4,5-trimethoxy-phenyl)-meth-(E)-ylidene]-hydrazine 
• 113628-51-6 N-(4-Chloro-phthalazin-1-yl)-N'-[1-(4-methoxy-3-methyl-phenyl)-meth-(E)-ylidene]-hydrazine 
• 87539-66-0 {3-Chloro-4-[(4-chloro-phthalazin-1-yl)-hydrazonomethyl]-phenyl}-dimethyl-amine 
• 87539-66-0 (3-Chloro-4-{[4-chloro-2H-phthalazin-(1Z)-ylidene]-hydrazonomethyl}-phenyl)-dimethyl-amine 
• 87539-63-7 N-[1-(3-Bromo-4,5-dimethoxy-phenyl)-meth-(E)-ylidene]-N'-(4-chloro-phthalazin-1-yl)-hydrazine 
• 87539-63-7 N-[1-(3-Bromo-4,5-dimethoxy-phenyl)-meth-(E)-ylidene]-N'-[4-chloro-2H-phthalazin-(1Z)-ylidene]-hydrazine 
• 113628-62-9 6-Chloro-3-(4-isopropoxy-phenyl)-[1,2,4]triazolo[3,4-a]phthalazine 
• 87539-64-8 N-(4-Chloro-phthalazin-1-yl)-N'-[1-(2,4,5-triethoxy-phenyl)-meth-(E)-ylidene]-hydrazine 
• 87539-64-8 N-[4-Chloro-2H-phthalazin-(1Z)-ylidene]-N'-[1-(2,4,5-triethoxy-phenyl)-meth-(E)-ylidene]-hydrazine 
• 87539-68-2 4-[(4-Chloro-phthalazin-1-yl)-hydrazonomethyl]-benzamide 
• 87539-62-6 N-(4-Chloro-phthalazin-1-yl)-N'-[1-(3,5-dibromo-2-ethoxy-phenyl)-meth-(E)-ylidene]-hydrazine 

Relevant articles and documents

Discovery of novel triazolophthalazine derivatives as DNA intercalators and topoisomerase II inhibitors

A new series of triazolophthalazine derivatives was designed and synthesized as topoisomerase II (Topo II) inhibitors and DNA intercalators. The synthesized derivatives were evaluated in vitro for their cytotoxic activities against three human cancer cell lines: HepG2, MCF-7, and HCT-116 cells. Compound IXb was the most potent counterpart with IC50 values of 5.39 ± 0.4, 3.81 ± 0.2, and 4.38 ± 0.3 μM, as it was about 1.47, 1.77, and 1.19 times more active than doxorubicin (IC50 = 7.94 ± 0.6, 6.75 ± 0.4, and 5.23 ± 0.3 μM) against HepG2, MCF-7, and HCT-116 cells, respectively. Additionally, the binding affinity of the synthesized compounds toward the DNA molecule was assessed using the DNA/methyl green assay. Compound?IXb showed an excellent DNA binding affinity with an IC50 value of 27.16 ± 1.2 μM, which was better than that of the reference drug doxorubicin (IC50 = 31.02 ± 1.80 μM). Moreover, compound IXb was the most potent member among the tested compounds when investigated for their Topo II inhibitory activity. Furthermore, compound IXb induced apoptosis in HepG2 cells and arrested the cell cycle at the G2/M phase. Additionally, compound IXb showed Topo II poisoning effects at 2.5 μM and Topo II catalytic inhibitory effects at 5 and 10 μM. Finally, molecular docking studies were carried out against the DNA–Topo II complex and DNA, to investigate the binding patterns of the designed compounds.

Design, synthesis, and antitumor activity of novel compounds based on 1,2,4-triazolophthalazine scaffold: Apoptosis-inductive and PCAF-inhibitory effects

The antitumor activity of newly synthesised triazolophthalazines (L-45 analogues) 10–32 was evaluated in human hepatocellular carcinoma (HePG-2), breast cancer (MCF-7), prostate cancer (PC3), and colorectal carcinoma (HCT-116) cells. Compounds 17, 18, 25, and 32 showed potent antitumor activity (IC50, 2.83–13.97 μM), similar to doxorubicin (IC50, 4.17–8.87 μM) and afatinib (IC50, 5.4–11.4 μM). HePG2 was inhibited by compounds 10, 17, 18, 25, 26, and 32 (IC50, 3.06–10.5 μM), similar to doxorubicin (IC50, 4.50 μM) and afatinib (IC50, 5.4 μM). HCT-116 and MCF-7 were susceptible to compounds 10, 17, 18, 25, and 32 (IC50, 2.83–10.36 and 5.69–11.36 μM, respectively), similar to doxorubicin and afatinib (IC50 = 5.23 and 4.17, and 11.4 and 7.1 μM, respectively). Compounds 17, 25, and 32 exerted potent activities against PC3 (IC50, 7.56–12.28 μM) compared with doxorubicin (IC50, 8.87 μM) and afatinib (IC50 7.7 μM). Compounds 17 and 32 were the strongest PCAF inhibitors (IC50, 5.31 and 10.30 μM, respectively) and compounds 18 and 25 exhibited modest IC50 values (17.09 and 32.96 μM, respectively) compared with bromosporine (IC50, 5.00 μM). Compound 17 was cytotoxic to HePG2 cells (IC50, 3.06 μM), inducing apoptosis in the pre-G phase and arresting the cell cycle in the G2/M phase. Molecular docking for the most active PCAF inhibitors (17 and 32) was performed.

Design, Synthesis, Molecular Docking, and Anticancer Activity of Phthalazine Derivatives as VEGFR-2 Inhibitors

Novel series of phthalazine derivatives 6–11 were designed, synthesized, and evaluated for their anticancer activity against two human tumor cell lines, HCT-116 human colon adenocarcinoma and MCF-7 breast cancer cells, targeting the VEGFR-2 enzyme. Compounds 7a,b and 8b,c showed the highest anticancer activities against both HCT116 human colon adenocarcinoma cells with IC50 of 6.04 ± 0.30, 13.22 ± 0.22, 18 ± 0.20, and 35 ± 0.45 μM, respectively, and MCF-7 breast cancer cells with IC50 of 8.8 ± 0.45, 17.9 ± 0.50, 25.2 ± 0.55, and 44.3 ± 0.49 μM, respectively, in comparison to sorafenib as reference drug with IC50 of 5.47 ± 0.3 and 7.26 ± 0.3 μM, respectively. Eleven compounds in this series were further evaluated for their inhibitory activity against VEGFR-2, where compounds 7a, 7b, 8c, and 8b also showed the highest VEGFR-2 inhibition with IC50 of 0.11 ± 0.01, 0.31 ± 0.03, 0.72 ± 0.08, and 0.91 ± 0.08 μM, respectively, in comparison to sorafenib as reference ligand with IC50 of 0.1 ± 0.02. Furthermore, molecular docking studies were performed for all synthesized compounds to predict their binding pattern and affinity towards the VEGFR-2 active site, in order to rationalize their anticancer activity in a qualitative way.