Apoptosis, ROS[1][2].
Epidermal growth factor targets the epidermal growth factor receptor (EGFR), a transmembrane receptor tyrosine kinase. Upon binding to EGFR, EGF induces receptor dimerization and autophosphorylation, activating downstream signaling pathways including the MAPK/ERK, PI3K/Akt, and PLCγ pathways. These pathways regulate cell proliferation, differentiation, survival, and migration. EGF signaling is essential for normal development and tissue homeostasis, and dysregulation of EGFR signaling is implicated in various cancers. EGF's ability to stimulate cell growth and proliferation makes it a key regulator of tissue development and repair. The receptor is also a major target for anticancer therapies.

In A431 cells, epidermal growth factor (EGF) (500 ng/mL; 0–20 minutes) might cause ROS generation [1]. A431 cells expressing exogenous catalase completely inhibited the tyrosine phosphorylation of several cellular proteins caused by epidermal growth factor (EGF) [1].
In vitro, EGF is a potent mitogen for a variety of epidermal and epithelial cells, including fibroblasts, glial cells, mammary epithelial cells, vascular and corneal endothelial cells, bovine granulosa cells, rabbit chondrocytes, HeLa cells, and SV40-3T3 cells. EGF stimulates cell proliferation, migration, and survival in these cell types. The EGF signaling pathway is involved in the regulation of apoptosis, with EGF promoting cell survival and protecting cells from apoptosis. In cell-based assays, EGF is used to study cell signaling, proliferation, and differentiation. The compound's effects on cell proliferation are concentration-dependent, with maximal effects observed at nanomolar concentrations.

In male mice, the application of 10 pg/day of epidermal growth factor (EGF) via an osmotic pump for eight days resulted in a highly substantial stimulatory effect on wound closure [3].
In vivo, EGF plays a critical role in development, tissue repair, and wound healing. EGF stimulates the proliferation and migration of epithelial cells, promoting wound closure and tissue regeneration. EGF is approved for the treatment of diabetic foot ulcers, where it is applied topically to promote wound healing. The compound also plays a role in gastrointestinal function, where it inhibits gastric acid secretion (as β-urogastrone). EGF is essential for normal development, as evidenced by the developmental abnormalities observed in EGF or EGFR knockout mice. The compound is also involved in cancer, where EGFR overexpression and mutation drive tumor growth and progression.

In vitro receptor binding assays for EGF are performed to assess its binding affinity for EGFR. The assay typically uses radiolabeled EGF (¹²⁵I-EGF) and cells or membranes expressing EGFR. The binding of ¹²⁵I-EGF to EGFR is measured in the presence of varying concentrations of unlabeled EGF. The dissociation constant (Kd) is determined from the competition binding curve. Surface plasmon resonance (SPR) or biolayer interferometry (BLI) can also be used to measure the binding affinity of EGF to purified EGFR. The assay includes positive controls (known EGFR ligands) and negative controls (vehicle or non-specific binding).

In vitro cell-based assays for EGF are performed using various cell lines that express EGFR. Cells are serum-starved to reduce background signaling and then treated with EGF at concentrations ranging from 0.1 to 100 ng/mL. EGFR phosphorylation is assessed by Western blotting using phospho-specific antibodies (e.g., anti-pEGFR Y1068). Downstream signaling (ERK, Akt phosphorylation) is also assessed. Cell proliferation is measured by BrdU incorporation, MTT assays, or cell counting. Cell migration is assessed using scratch wound or transwell assays. Apoptosis is assessed by flow cytometry or caspase activity assays. EGF's effects on gene expression are assessed by qRT-PCR or microarray analysis.

Animal/Disease Models: C57BL6J and CBA mice (0.5-cm2 full-thickness back wound was cut out of the center of the back)[3]
Doses: 10 μg /day
Route of Administration: Osmotic pump delivered over 8 days at 10 pg/day
Experimental Results: demonstrated a highly significant (P < 0.001) stimulatory effect on wound closure over 6 days in male mice.
In vivo animal studies with EGF are conducted in models of wound healing, gastrointestinal function, and cancer. For wound healing, EGF is applied topically to wounds in mice or rats, and wound closure is monitored. For gastrointestinal studies, EGF is administered orally or intravenously, and gastric acid secretion is measured. In cancer models, the effects of EGF on tumor growth are studied, often in the context of EGFR-targeted therapies. EGF is also used to study developmental processes in animal models. The compound's efficacy and safety in vivo depend on the route of administration, dose, and the specific biological context.

EGF is a polypeptide that is rapidly cleared from the circulation. Following administration, EGF binds to EGFR on target cells and is internalized and degraded. The compound has a short half-life in the circulation, typically on the order of minutes. EGF is metabolized by proteolytic enzymes in tissues and is excreted as small peptides and amino acids. The pharmacokinetics of EGF depend on the route of administration, with topical application resulting in local effects and minimal systemic exposure. For research use, EGF is typically formulated in sterile buffers and stored at -20°C to maintain stability.

EGF is generally well-tolerated at therapeutic doses. Topical application of EGF for wound healing is safe and effective, with minimal systemic absorption and low risk of adverse effects. Systemic administration of EGF may cause gastrointestinal effects, including nausea, vomiting, and diarrhea. EGF may also stimulate the growth of EGFR-expressing tumors, and its use is contraindicated in patients with known malignancies. As a research reagent, EGF is handled with standard laboratory precautions. The compound is for research use only and not for human therapeutic applications outside approved clinical use.

[1]. Bae YS, et al. Epidermal growth factor (EGF)-induced generation of hydrogen peroxide. Role in EGF receptor-mediated tyrosine phosphorylation. J Biol Chem. 1997 Jan 3;272(1):217-21.
[2]. Henson ES, Gibson SB. Surviving cell death through epidermal growth factor (EGF) signal transduction pathways: implications for cancer therapy. Cell Signal. 2006 Dec;18(12):2089-97.
[3]. Niall M, Ryan GB, O'Brien BM. The effect of epidermal growth factor on wound healing in mice. J Surg Res. 1982 Aug;33(2):164-9.

Nepidermin is a recombinant form of the naturally occurring polypeptide human epidermal growth factor (rhEGF) with potential epithelial regeneration and cell-protective activity. Topical application of recombinant human epidermal growth factor (rhEGF) can stimulate epithelial cell proliferation, differentiation, and migration, thereby accelerating epithelial regeneration and wound healing. Furthermore, rhEGF can reduce chemotherapy- and/or radiotherapy-related epithelial cell toxicity.
See also: Human Epidermal Growth Factor (note moved to).
Epidermal growth factor is a key regulator of cell proliferation, differentiation, and survival, and plays a critical role in normal development, tissue repair, and cancer. The EGF signaling pathway is one of the most extensively studied signaling pathways in biology and is a major target for anticancer therapies, including EGFR inhibitors and monoclonal antibodies such as cetuximab and panitumumab. EGF's role in wound healing has led to its clinical use for the treatment of diabetic foot ulcers and other chronic wounds. The compound is also used in cell culture as a growth supplement for various cell types. EGF is available from chemical suppliers for research purposes.

C270H401N73O83S7

6221.96723999994

6219.751

62253-63-8

Epidermal growth factor (EGF) (phosphate)

16143379

Typically exists as solid at room temperature

-17.3

94

98

203

433

15800

51

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GVUGOAYIVIDWIO-UFWWTJHBSA-N

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(4S)-5-[[(2S)-1-[[(2R)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(1S)-4-carbamimidamido-1-carboxybutyl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxo-3-sulfanylpropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-[[2-[[(2S,3S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2R)-2-[[(2S)-4-amino-2-[[(2R)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-3-carboxy-2-[[(2S)-2-[[(2S)-2-[[(2S)-4-carboxy-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2R)-2-[[(2S)-2-[[2-[[(2S)-3-carboxy-2-[[(2S)-2-[[(2S)-2-[[(2R)-2-[[(2S)-2-[[2-[[(2S)-3-carboxy-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2R)-2-[[(2S)-4-carboxy-2-[[(2S)-2-[[(2S)-3-carboxy-2-[[(2S)-2-[[(2S)-2,4-diamino-4-oxobutanoyl]amino]-3-hydroxypropanoyl]amino]propanoyl]amino]-3-hydroxypropanoyl]amino]butanoyl]amino]-3-sulfanylpropanoyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]propanoyl]amino]acetyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-sulfanylpropanoyl]amino]-4-methylpentanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]propanoyl]amino]acetyl]amino]-3-methylbutanoyl]amino]-3-sulfanylpropanoyl]amino]-4-methylsulfanylbutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-methylpentanoyl]amino]butanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]propanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]propanoyl]amino]-3-sulfanylpropanoyl]amino]-4-oxobutanoyl]amino]-3-sulfanylpropanoyl]amino]-3-methylbutanoyl]amino]-3-methylbutanoyl]amino]acetyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-5-oxopentanoic acid

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)

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

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.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*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).

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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)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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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).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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