448-97-5

Basic information

• Product Name: 3,3'-difluorobenzidine
• Synonyms: 3,3'-difluorobenzidine;4,4’-Diamino-3,3’-difluorobiphenyl;3,3'-Difluorobiphenyl-4,4'-diamine;3,3'-Difluoro-[1,1'-biphenyl]-4,4'-diaMine
• CAS NO: 448-97-5
• Molecular Formula: C₁₂H₁₀F₂N₂
• Molecular Weight: 220.22
• Mol File: 448-97-5.mol

Chemical Properties

• Boiling Point: 335.8°Cat760mmHg
• Flash Point: 152.2°C
• Appearance: /
• Density: 1.313g/cm³
• Storage Temp.: 2-8°C
• CAS DataBase Reference: 3,3'-difluorobenzidine(CAS DataBase Reference)
• NIST Chemistry Reference: 3,3'-difluorobenzidine(448-97-5)
• EPA Substance Registry System: 3,3'-difluorobenzidine(448-97-5)

Safety Data

• Hazardous Substances Data: 448-97-5(Hazardous Substances Data)

Usage

Uses

4,4''-Diamino-3,3''-difluorobiphenyl

Upstream product

• 401-44-5 2,2'-difluoroazobenzene 
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• 454-21-7 1,2-bis(2-fluorophenyl)hydrazine 

Relevant articles and documents

Blue-colored donor-acceptor [2]rotaxane

Equation presented A guest molecule - a bis-N-tetraethyleneglycol- substituted 3,3′-difluorobenzidine derivative - has been synthesized, and its complexation with the host, cyclobis(paraquat-p-phenylene), has been investigated. This host-guest complex was then employed in the template-directed synthesis of a blue-colored [2]rotaxane. The color of this [2]rotaxane arises from the charge-transfer absorption band between the HOMO of the guest and the LUMO of the host. This host-guest complex, and the derived [2]rotaxane, completes the donor-acceptor-based RGB (red/green/blue) color complex set.

Design, synthesis and biological evaluation of small-azo-dyes as potent Vesicular Glutamate Transporters inhibitors

Vesicular Glutamate Transporters (VGLUTs) allow the loading of presynapic glutamate vesicles and thus play a critical role in glutamatergic synaptic transmission. VGLUTs have proved to be involved in several major neuropathologies and directly correlated to clinical dementia in Alzheimer and Parkinson's disease. Accordingly VGLUT represent a key biological target or biomarker for neuropathology treatment or diagnostic. Yet, despite the pivotal role of VGLUTs, their pharmacology appears quite limited. Known competitive inhibitors are restricted to some dyes as Trypan Blue (TB) and glutamate mimics. This lack of pharmacological tools has heavily hampered VGLUT investigations. Here we report a rapid access to small molecules that combine benefits of TB and dicarboxylic quinolines (DCQs). Their ability to block vesicular glutamate uptake was evaluated. Several compounds displayed low micromolar inhibitory potency when size related compounds are thirty to forty times less potent (i.e. DCQ). We then confirmed the VGLUT selectivity by measuring the effect of the series on vesicular monoamine transport and on metabotropic glutamate receptor activity. These inhibitors are synthesized in only two steps and count among the best pharmacological tools for VGLUTs studies.

ortho-Substituent effects on the in vitro and in vivo genotoxicity of benzidine derivatives

Benzidine and its 3,3'-diamino, 3,3'-dimethyl, 3,3'-dimethoxy, 3,3'-difluoro, 3,3'-dichloro, 3,3'-dibromo, 3,3'-dicarbomethoxy and 3,3'-dinitro derivatives together with 2-nitrobenzidine and 3-nitrobenzidine were compared for their in vitro and in vivo genotoxicity. Relative mutagenicity was established with Salmonella strains TA98, TA98/1,8-DNP6 and TA100 with and without S9 activation. All the derivatives in the presence of S9 were more mutagenic than benzidine with 3,3'-dinitro- and 3-nitro-benzidine having the greatest mutagenicity. Mutagenicity in all 3 strains with S9 activation could be correlated to electron-withdrawing ability of substituent groups, as measured by the basicity of the amines. This correlation was explained on the basis that electron-withdrawing groups could favor the stability of the mutagenic intermediate N-hydroxylamine and also enhance the reactivityof the ultimate mutagenic species, the nitrenium ion. Mutagenicity was also correlated to the energy of the lowest unoccupied molecular orbitals (E(LUMO)). Hydrophibicity was found to have very limited effect on the relative mutagenicity of our benzidine derivatives. The in vivo endpoint was chromosomal aberrations in the bone-marrow cells of mice following intraperitoneal administration of benzidine and its derivatives. In contrast to the in vitro results, while all the amines were genotoxic in vivo, only the 3-nitro derivative had a significant increase in toxicity over benzidine.