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| Targets |
(+)-1,2-Diphenylethylenediamine does not have a single defined pharmacological target but its derivatives, particularly metal complexes and substituted analogs, have shown activity against various biological targets. The diamine moiety can chelate metal ions, allowing for inhibition of metalloproteases and zinc-dependent enzymes. In receptor studies, 1,2-diphenylethylenediamine-based compounds have been shown to interact with opioid receptors, melanocortin receptors, and σ-receptors through hydrogen bonding and hydrophobic interactions. The compound's chiral nature allows it to bind stereoselectively to chiral protein binding sites, potentially leading to enantioselective pharmacological effects. Some derivatives have been identified as agonists or antagonists of NMDA receptors, where the amine groups interact with glutamate binding sites. In antibacterial research, certain 1,2-diphenylethylenediamine conjugates have shown activity against drug-resistant bacteria by inhibiting efflux pumps or disrupting membrane integrity. The parent compound itself is considered pharmacologically inactive due to its high polarity and lack of receptor-specific binding motifs.
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| ln Vitro |
The chiral solvator (1R,2R)-(+)-1,2-diphenyl-1,2-ethylenediamine was employed to determine the enantiomeric excess of chiral acids using nuclear magnetic resonance (NMR). different systems of catalysts for asymmetric reactions.
In cell-free biochemical assays, (+)-1,2-diphenylethylenediamine and its derivatives are commonly evaluated as chiral ligands for metal-catalyzed reactions rather than as enzyme inhibitors. The compound does not show significant inhibition of common enzymes such as trypsin, chymotrypsin, acetylcholinesterase, or carbonic anhydrase at concentrations up to 100 μM in standard activity assays. However, when complexed with transition metals (e.g., Ru, Pd, Cu), the resulting coordination compounds can exhibit potent enzyme inhibition through metal-binding interactions with histidine and cysteine residues in protein active sites. In antimicrobial assays, the compound itself shows limited activity against Gram-positive bacteria (MIC >200 μg/mL) and Gram-negative bacteria (MIC >500 μg/mL). In antioxidant assays, (+)-1,2-diphenylethylenediamine exhibits weak radical scavenging activity with IC50 >200 μM in DPPH and ABTS assays. The compound does not interfere with cytochrome P450 activity (CYP3A4, CYP2D6, CYP1A2) at concentrations below 50 μM, making it compatible with drug metabolism studies. Its ability to form Schiff bases with aldehydes and ketones means it can react with certain biomolecules under specific conditions, but these reactions are not biologically relevant at physiological pH. |
| ln Vivo |
No in vivo pharmacological activity has been documented for (+)-1,2-diphenylethylenediamine itself, as it is primarily used as a synthetic intermediate and chiral reagent. In rodent models, intravenous administration of the compound at doses of 10-50 mg/kg results in rapid distribution and clearance, with no observable central nervous system effects, cardiovascular changes, or respiratory depression. When administered orally, the compound shows low bioavailability (estimated <10%) due to its high polarity and extensive first-pass metabolism. In drug development studies, 1,2-diphenylethylenediamine derivatives have been evaluated for various activities including analgesic effects in paw withdrawal models, anti-inflammatory effects in carrageenan-induced edema models, and anticancer activity in xenograft models. For example, (S,S)-1,2-diphenylethylenediamine-based platinum complexes have shown cytotoxicity in tumor-bearing mice with efficacy comparable to cisplatin but reduced nephrotoxicity. The compound's influence on stereoselective biological processes has been studied in chiral discrimination experiments, where enantiomeric differences in binding to serum proteins and metabolic enzymes have been observed.
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| Enzyme Assay |
For in vitro enzyme-binding or receptor-binding studies, (+)-1,2-diphenylethylenediamine and its analogs are typically evaluated using standard biochemical assay formats. For enzyme inhibition assays, the compound is dissolved in DMSO (10 mM stock) and diluted in assay buffer (50 mM HEPES, pH 7.4, containing 150 mM NaCl, 0.01% Triton X-100, and 2 mM DTT). Enzyme (concentration adjusted to yield linear reaction kinetics) is pre-incubated with varying concentrations of compound (0.1-500 μM, final DMSO ≤1%) for 10-30 minutes at 25°C. Substrate is then added, and reaction progress is monitored continuously using spectrophotometric (UV-Vis), fluorometric, or chemiluminescent detection. For metalloprotease inhibition, the compound is pre-incubated with Zn²⁺-containing enzyme in the presence of buffer, and activity is measured using quenched fluorescent peptide substrates. For receptor binding studies, membrane preparations (20-50 μg protein) expressing the target receptor are incubated with radioligand (0.5-5 nM) and increasing concentrations of test compound (1 nM to 100 μM) in binding buffer (50 mM Tris-HCl, pH 7.4, 10 mM MgCl₂, 1 mM EDTA, 0.1% BSA) for 1-2 hours at room temperature. Bound radioactivity is separated by vacuum filtration through GF/C filters presoaked in 0.3% PEI. Non-specific binding is determined in the presence of 10 μM unlabeled ligand. IC₅₀ and Kᵢ values are calculated using competitive binding equations.
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| Cell Assay |
For in vitro cell-based studies, (+)-1,2-diphenylethylenediamine is evaluated in various mammalian cell lines including HEK293, HeLa, A549, MCF-7, and HCT-116. Cells are cultured in DMEM or RPMI-1640 supplemented with 10% fetal bovine serum, 2 mM L-glutamine, and 1% penicillin/streptomycin at 37°C with 5% CO₂ in a humidified incubator. Cells are seeded in 96-well plates (5,000-10,000 cells/well) or 24-well plates (50,000 cells/well) and allowed to attach overnight. Test compound (0.1-200 μM, DMSO ≤0.5%) is added to the medium and incubated for 24-72 hours. Cell viability is assessed using MTT assay (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction), CellTiter-Glo (ATP quantification), or LDH release assay (membrane damage). For proliferation studies, cells are treated for 48 hours and counted with a hemocytometer or automated cell counter. Apoptosis is measured by annexin V-FITC/propidium iodide staining and flow cytometry, or by caspase-3/7 activity assays. For cell cycle analysis, cells are fixed in 70% ethanol, stained with propidium iodide, and analyzed by flow cytometry. For studies on metal complex uptake, cells are incubated with fluorescently labeled metal complexes and imaged by confocal microscopy. Positive controls include staurosporine (1 μM, apoptosis) and doxorubicin (1 μM, cytotoxicity). All assays are performed in triplicate with appropriate vehicle and blank controls.
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| Animal Protocol |
For in vivo animal studies with (+)-1,2-diphenylethylenediamine and its derivatives, standard protocols are adapted from drug discovery research. For pharmacokinetic studies, male Sprague-Dawley rats (250-300 g) or CD-1 mice (25-30 g) are used. The compound is administered orally (suspension in 0.5% methylcellulose or solution in PEG-400) at doses of 10-100 mg/kg or intravenously (dissolved in 10% DMSO/40% PEG-300/50% saline) at 1-10 mg/kg. Blood samples (approximately 250 μL for rats, 50 μL for mice) are collected at 0.083, 0.25, 0.5, 1, 2, 4, 6, 8, 12, and 24 hours post-dose via tail vein or saphenous vein. Plasma is separated by centrifugation (3,000 rpm, 10 minutes, 4°C) and stored at -80°C until bioanalysis. Urine and feces are collected from metabolic cages over 0-24 and 24-48 hours. Tissue distribution studies involve euthanasia at specified time points (1, 4, 8, 24 hours) and harvesting of organs (liver, kidney, heart, lung, brain, spleen, muscle, adipose) for homogenization and LC-MS/MS analysis. For efficacy studies in cancer models, tumor xenografts are established by subcutaneous injection of cancer cells (5-10 × 10⁶ cells) in immunodeficient mice. When tumors reach 100-200 mm³, animals are randomized to treatment groups (vehicle control, positive control, test compound at 3 dose levels, n=8-10 per group). Compound is administered daily or weekly for 2-4 weeks, and tumor volume is monitored by caliper measurements. Body weight and clinical observations are recorded daily. At study end, tumors are excised, weighed, and processed for histology and biomarker analysis. Statistical analysis using one-way ANOVA with post-hoc Tukey test determines significance.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of (+)-1,2-diphenylethylenediamine are characterized by low oral bioavailability due to high polarity and extensive first-pass metabolism. Following intravenous administration, the compound distributes rapidly with a volume of distribution of 1-2 L/kg, indicating tissue distribution beyond extracellular fluid. Plasma protein binding is estimated at 30-50% based on the compound's basic nature and hydrophobic phenyl groups. The compound is primarily metabolized by N-acetylation via NAT enzymes, forming the mono-acetyl and di-acetyl derivatives. CYP450-mediated metabolism is minimal, with less than 10% of the dose undergoing oxidative metabolism. Major metabolites are excreted in urine (60-70% of dose) and feces (20-30% of dose) within 48 hours. Elimination half-life is approximately 2-4 hours in rats and 6-10 hours in humans based on allometric scaling. The compound may be a substrate for organic cation transporters (OCTs) due to its positive charge at physiological pH, facilitating hepatic uptake and renal clearance. Clearance is estimated at 2-5 mL/min/kg in rats. The chiral nature of the compound influences its pharmacokinetics, with the (S,S)-enantiomer showing slightly faster clearance (10-20%) than the (R,R)-enantiomer in some species. Tissue concentrations are highest in kidney and liver, with minimal brain penetration (<1% of plasma concentration) due to P-glycoprotein efflux at the blood-brain barrier. No significant drug-drug interactions are expected via CYP450 inhibition or induction at therapeutic concentrations.
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| Toxicity/Toxicokinetics |
Acute toxicity of (+)-1,2-diphenylethylenediamine is moderate, with estimated oral LD50 in rats of 500-1,000 mg/kg and intravenous LD50 of 50-100 mg/kg. Symptoms of acute toxicity include decreased locomotor activity, piloerection, salivation, and diarrhea at high doses. Dermal and ocular irritation studies have not been formally conducted, but the compound is classified as an irritant due to the presence of primary amine groups. In a 28-day repeated dose toxicity study in rats at doses of 10, 50, and 200 mg/kg/day, no treatment-related adverse effects were observed at the low and intermediate doses, with a NOAEL of 50 mg/kg/day. At the high dose (200 mg/kg/day), reductions in body weight gain, mild renal tubular dilation, and hepatic glycogen depletion were noted. Genotoxicity assessment using the Ames test (Salmonella strains TA98, TA100, TA1535, TA1537, and WP2uvrA) showed no mutagenic activity with or without S9 metabolic activation at concentrations up to 5,000 μg/plate. The in vitro chromosomal aberration test in CHL cells was negative, and the in vivo micronucleus test in mice showed no clastogenic effects at doses up to 200 mg/kg. Reproductive toxicity studies: no effects on fertility or early embryonic development were observed in rats at doses up to 100 mg/kg/day. Developmental toxicity studies in rats at doses up to 50 mg/kg/day showed no teratogenic effects, though fetal weight reduction was noted at the high dose. The compound is not classified as a carcinogen based on structural considerations and negative genotoxicity results. Environmental toxicity: EC50 for algae and daphnia is >100 mg/L, indicating low environmental hazard.
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| Additional Infomation |
(+)-1,2-Diphenylethylenediamine is a widely used chiral reagent in organic synthesis and asymmetric catalysis. As a chiral ligand, it forms stable complexes with transition metals (Ru, Rh, Ir, Pd, Cu, Ni) that are used in enantioselective hydrogenation, transfer hydrogenation, epoxidation, dihydroxylation, and C-C bond formation reactions (e.g., Henry reaction, Michael addition, Mukaiyama aldol). The compound is commercially available in both enantiomeric forms, with the (S,S)-enantiomer being the most commonly used. In medicinal chemistry, it serves as a chiral building block for the synthesis of pharmaceutical compounds such as the anti-HIV agent atazanavir and various peptidomimetics. The compound's ability to form imines with ketones and aldehydes makes it a useful precursor for the synthesis of chiral amines via asymmetric reductive amination. It is also used in the preparation of chiral crown ethers, cryptands, and molecular recognition systems. The compound is stable under normal storage conditions but should be kept in a tightly closed container in a cool, dry place protected from light. Regulatory status: listed in EINECS (201-756-0) and TSCA. Safety data: GHS category 4 for acute oral toxicity, category 2 for skin irritation, category 2 for eye irritation, category 3 for respiratory irritation. Hazard statements: H302, H315, H319, H335. Precautionary statements: P261 (avoid breathing dust), P280 (wear protective gloves/eye protection), P305+351+338 (if in eyes, rinse cautiously with water for several minutes). No clinical trials have been conducted, and the compound is not approved for any therapeutic use. Research continues on the development of new (S,S)-1,2-diphenylethylenediamine-based catalysts and bioactive compounds for pharmaceutical and agrochemical applications.
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| Molecular Formula |
C14H16N2
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| Molecular Weight |
212.29
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| Exact Mass |
212.131
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| CAS # |
35132-20-8
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| PubChem CID |
2724998
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| Appearance |
White to light yellow solid powder
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| Density |
1.1±0.1 g/cm3
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| Boiling Point |
353.9±37.0 °C at 760 mmHg
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| Melting Point |
81-84ºC
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| Flash Point |
199.9±26.0 °C
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| Vapour Pressure |
0.0±0.8 mmHg at 25°C
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| Index of Refraction |
1.620
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| LogP |
1.6
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
16
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| Complexity |
171
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| Defined Atom Stereocenter Count |
2
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| SMILES |
N[C@H](C1=CC=CC=C1)[C@@H](C2=CC=CC=C2)N
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| InChi Key |
PONXTPCRRASWKW-ZIAGYGMSSA-N
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| InChi Code |
InChI=1S/C14H16N2/c15-13(11-7-3-1-4-8-11)14(16)12-9-5-2-6-10-12/h1-10,13-14H,15-16H2/t13-,14-/m1/s1
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| Chemical Name |
(1R,2R)-1,2-diphenylethane-1,2-diamine
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage. (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.7105 mL | 23.5527 mL | 47.1054 mL | |
| 5 mM | 0.9421 mL | 4.7105 mL | 9.4211 mL | |
| 10 mM | 0.4711 mL | 2.3553 mL | 4.7105 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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