Benzoin targets the phosphoinositide 3-kinase alpha (PI3Kα) signaling pathway. PI3Kα is a lipid kinase involved in cell growth, proliferation, survival, and metabolism, and is frequently dysregulated in cancer. Benzoin acts as a PI3Kα inhibitor, blocking the phosphorylation of downstream effectors including AKT. By inhibiting PI3Kα signaling, Benzoin reduces cell proliferation and induces cell death in cancer cells. The compound is also an EC 3.1.1.1 (carboxylesterase) inhibitor.

In vitro, Benzoin demonstrates anticancer effects by inhibiting the growth of colon cancer cell lines, particularly HCT-116 cells. The compound shows antiproliferative activity with a 24-hour treatment period. Benzoin inhibits PI3Kα activity, leading to reduced AKT phosphorylation and downstream signaling. The compound's activity is concentration-dependent, with effects observed at micromolar concentrations. In cell-based assays, Benzoin reduces cell viability and induces apoptosis in cancer cells. The compound's mechanism involves disruption of the PI3K/AKT/mTOR signaling axis.

In vivo, Benzoin's anticancer activity has been studied in preclinical models. As a PI3Kα inhibitor, Benzoin has the potential to suppress tumor growth in animal models of colon cancer and other PI3K-dependent malignancies. However, detailed in vivo efficacy data are limited. The compound's natural resin origin and historical use as a food additive and colorant provide some preliminary safety information. Further preclinical studies are needed to fully characterize the in vivo anti-tumor activity and therapeutic potential of Benzoin.

Non-cell-based assays for Benzoin include kinase inhibition assays to measure PI3Kα activity. Recombinant PI3Kα enzyme is incubated with Benzoin at various concentrations, and kinase activity is measured using a luminescent or fluorescence-based assay that detects ATP consumption or product formation. IC₅₀ values are calculated from dose-response curves. Binding affinity of Benzoin to PI3Kα can be measured using surface plasmon resonance or isothermal titration calorimetry. Competitive binding assays with ATP are used to determine the mode of inhibition. For carboxylesterase inhibition, enzymatic activity is measured using p-nitrophenyl acetate as a substrate.

Cellular assays for Benzoin are performed using cancer cell lines including HCT-116 (colon cancer). Cells are treated with Benzoin at various concentrations for specified time points (e.g., 24 hours), and cell viability is measured by MTT, CellTiter-Glo, or SRB assays. Apoptosis is assessed by Annexin V/PI staining, caspase activation, or DNA fragmentation. PI3K/AKT pathway inhibition is confirmed by Western blot analysis of phospho-AKT and downstream targets (mTOR, p70S6K). Cell cycle analysis is performed by flow cytometry. Anti-proliferative activity is quantified by colony formation assays.

In vivo efficacy of Benzoin is evaluated in mouse xenograft models using colon cancer cell lines. Mice are implanted subcutaneously with tumor cells and, when tumors reach a specified size, treated with Benzoin via oral or intraperitoneal administration. Tumor volume is measured longitudinally, and tumor growth inhibition is calculated. Tumor tissues are harvested for histology and pharmacodynamic analysis including PI3K/AKT pathway inhibition and assessment of apoptosis and proliferation markers. Body weight and clinical signs are monitored for tolerability. However, detailed in vivo data for Benzoin as a pure compound are limited.

Absorption, Distribution and Excretion
No pharmacokinetic data. No pharmacokinetic data. No pharmacokinetic data. No pharmacokinetic data. Metabolites/Metabolites No pharmacokinetic data. Benzoic acid is converted to hydrobenzoic acid and meso-hydrobenzoic acid in Curvularia. ACKLIN, W et al., Croatian Journal of Chemistry, 37, 11 (1965). /Excerpt from Tables/ Biological Half-Life No pharmacokinetic data.

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Pharmacokinetic properties of Benzoin have not been extensively characterized. As a small organic compound with moderate lipophilicity, Benzoin is expected to be absorbed after oral administration. The compound is metabolized primarily in the liver, and its major metabolic pathway involves oxidation to benzil. The compound's half-life, bioavailability, and tissue distribution are not well-defined. In research settings, Benzoin is typically used as a tool compound rather than a therapeutic agent, and comprehensive PK studies are lacking.

Protein Binding

No pharmacokinetic data available.

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The toxicity of Benzoin has been evaluated in the context of its use as a food additive and colorant. Benzoin is generally recognized as safe at low concentrations when used as a food additive. However, at pharmacological doses, the compound may have cytotoxic effects due to its PI3Kα inhibitory activity. In vitro, Benzoin shows antiproliferative activity against cancer cells, indicating potential cytotoxicity. Comprehensive toxicological studies including genotoxicity, cardiotoxicity, and organ toxicity are lacking. As with all PI3K inhibitors, there is potential for metabolic and endocrine side effects.

[1]. COMPOUND SUMMARY. Benzoin.

Benzoin is a grayish-white to yellowish-white crystalline solid with a camphor odor and a slightly pungent taste. When broken, the fresh surface is milky white. (NTP, 1992)
Benzoin is a ketone compound composed of acetophenone with a hydroxyl group and a phenyl substituent at the α-position. It is the parent compound of the benzoin class. It is an EC 3.1.1.1 (carboxylesterase) inhibitor. It is a member of the benzoin class and also a secondary α-hydroxy ketone.
Benzoin is a white crystalline compound prepared by the condensation of benzaldehyde in potassium cyanide and used in organic synthesis. Do not confuse it with benzoin gum produced by STYRAX (see [DB11222]). Benzoin is a colorant approved by the U.S. Food and Drug Administration (FDA) for labeling fruits and vegetables.
Benzoin has been reported in Dianthus caryophyllus, and relevant data exists. (±)-Benzoin is a flavoring agent. Benzoin is an organic compound with the molecular formula PhCH(OH)C(O)Ph. It is a hydroxyketone linked by two phenyl groups. It is a grayish-white crystalline solid with a slightly camphor-like odor. Benzoin is synthesized from benzaldehyde via the benzoin condensation reaction. It is chiral and exists in two enantiomers: (R)-benzoin and (S)-benzoin. (Wikipedia)
Benzoin belongs to the benzoin family of compounds. These are organic compounds containing a 1,2-hydroxyketone linked by two phenyl groups.
Benzoin is a metabolite of or produced by Saccharomyces cerevisiae.
It is a white crystalline compound obtained by the condensation of benzaldehyde in potassium cyanide and is used in organic synthesis. Do not confuse it with the benzoin gum of benzoin (STYRAX). See also: Siamese benzoin gel (note moved to); benzoin resin (note moved to).

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Drug indications
There are currently no approved therapeutic indications.

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Benzoin (CAS# 119-53-9) is a natural balsamic resin with the molecular formula C₁₄H₁₂O₂ and a molecular weight of 212.24. It is a PI3Kα inhibitor with anticancer effects, inhibiting the growth of colon cancer cell lines including HCT-116. Benzoin is also used as a precursor to benzil (a photoinitiator) and as a color additive. The compound is known as DL-Benzoin, Desyl alcohol, and (±)-2-Hydroxy-2-phenylacetophenone. As of current knowledge, Benzoin is not approved as a therapeutic agent but is used in research for its PI3K inhibitory activity.

C14H12O2

212.24

212.083

119-53-9

Benzoin-d10;56830-64-9

8400

White to off-white solid powder

1.2±0.1 g/cm3

343.0±0.0 °C at 760 mmHg

279 °F (NTP, 1992) ; 134-138 ; MP:133-4 °C /D & L FORMS/ ; 137 °C ; 137 °C

154.8±14.9 °C

0.0±0.8 mmHg at 25°C

1.609

2.13

1

2

3

16

225

0

C1=CC=C(C=C1)C(C(=O)C2=CC=CC=C2)O

ISAOCJYIOMOJEB-UHFFFAOYSA-N

InChI=1S/C14H12O2/c15-13(11-7-3-1-4-8-11)14(16)12-9-5-2-6-10-12/h1-10,13,15H

2-hydroxy-1,2-diphenylethanone

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 50 mg/mL (235.58 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (11.78 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (11.78 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (11.78 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)