KGF (Keratinocyte Growth Factor)

KGF (FGF-7) is a 163-amino acid growth factor that specifically targets keratinocytes via the FGFR2-IIIb receptor, with clinical applications in mucositis treatment, wound healing, and hair follicle biology.

KGF (Keratinocyte Growth Factor), also known as FGF-7, is a 163-amino acid member of the fibroblast growth factor family that acts specifically on epithelial cells through the FGFR2-IIIb receptor. Unlike most FGFs, KGF exhibits remarkable cell-type specificity -- it is produced exclusively by mesenchymal cells (fibroblasts, endothelial cells, smooth muscle cells) and acts exclusively on epithelial cells (keratinocytes).

Overview

KGF was first identified in 1989 from conditioned media of human embryonic lung fibroblasts. It is a natural paracrine mediator of epithelial growth and differentiation, with expression dramatically upregulated (up to 160-fold) during wound healing. The recombinant form, palifermin (Kepivance), is FDA-approved for the prevention of severe oral mucositis in hematologic malignancy patients undergoing myeloablative therapy and stem cell transplantation. Beyond oncology, KGF is studied for its protective effects on epithelial tissues of the skin, lungs, gastrointestinal tract, and bladder. In cosmetics, biosynthetic KGF is used in formulations targeting skin barrier repair and hair growth.

Mechanism of Action

KGF binds with high affinity to FGFR2-IIIb (also called KGFR), a splice variant of the FGF receptor 2 expressed almost exclusively on epithelial cells. Receptor binding triggers dimerization and activation of intracellular tyrosine kinase domains, initiating the RAS-MAPK and PI3K-AKT signaling cascades. These pathways drive keratinocyte proliferation, migration, and differentiation while simultaneously upregulating anti-apoptotic factors (Bcl-2, Bcl-xL) and cytoprotective enzymes (Nrf2 pathway). KGF also stimulates production of detoxifying enzymes in epithelial cells, providing protection against reactive oxygen species and cytotoxic agents. The strict epithelial specificity of FGFR2-IIIb ensures that KGF does not stimulate fibroblast or endothelial cell proliferation, reducing concerns about fibrosis or aberrant angiogenesis Finch & Rubin (2004).

Reconstitution Calculator

KGF (Keratinocyte Growth Factor)

**KGF (Keratinocyte Growth Factor)**, also known as FGF-7, is a 163-amino acid m

Draw Volume
0.019mL
Syringe Units
2units
Concentration
3,125mcg/mL
Doses / Vial
104doses
Vial Total
6mg
Waste / Vial
10mcg
Syringe Cap.
100units · 1mL
Recommended Schedule
M
T
W
T
F
S
S
FrequencyOnce daily x6 doses total
How to reconstitute
Gather & prepare
1/6Gather & prepare

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2.Your 6.25mg peptide vial (lyophilized powder)
3.Bacteriostatic water (you'll need 2mL)
4.A 3–5mL syringe with 21–25 gauge needle for reconstitution
5.Alcohol swabs (70% isopropyl)
Use bacteriostatic water (0.9% benzyl alcohol) for multi-dose vials. Sterile water is only safe for single-use.
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27%
1vial
28 doses104 days/vial76 leftover
Cost Breakdown
Vial price
$0.00per dose
$0.00 /week$0 /month
Store 2-8°C30 day shelf lifeSwirl gentlyFor research purposes only

Research

Mucositis Prevention (FDA-Approved)

Palifermin is FDA-approved for prevention of severe oral mucositis in patients with hematologic malignancies receiving myeloablative conditioning regimens followed by autologous stem cell transplantation. In pivotal clinical trials, palifermin reduced the incidence of WHO grade 3-4 oral mucositis from 98% to 63% and shortened the duration of severe mucositis by 3 days compared to placebo. Patients reported significantly less oral pain, reduced need for opioid analgesics, and improved ability to eat and drink Spielberger et al. (2004).

Wound Healing

KGF expression increases up to 160-fold at wound sites within 24 hours of injury, making it one of the most dramatically upregulated factors in the wound healing response. Exogenous KGF accelerates re-epithelialization by stimulating keratinocyte proliferation at wound margins and promoting migration across the wound bed. In animal models, topical KGF application has demonstrated accelerated closure of full-thickness wounds, improved epithelial barrier function, and enhanced tensile strength of healed tissue. KGF is particularly effective in impaired healing models, including diabetic wounds and radiation-damaged skin Werner (1998).

Hair Follicle Biology

FGFR2-IIIb is expressed in the outer root sheath and matrix cells of hair follicles, and KGF signaling plays a critical role in hair follicle morphogenesis and cycling. KGF promotes proliferation of follicular keratinocytes during the anagen (growth) phase and protects the follicular epithelium from apoptosis during catagen. Topical and injectable KGF formulations have shown promise in stimulating hair growth in androgenetic alopecia research models. KGF also protects hair follicles from chemotherapy-induced damage, with preclinical studies demonstrating preservation of hair follicle structure when KGF is administered prior to cytotoxic agents Danilenko et al. (1995)80002-6).

Radiation Protection

KGF protects epithelial tissues from radiation injury by stimulating proliferation of progenitor cells and upregulating DNA repair and antioxidant enzymes. In radiation therapy patients, palifermin has reduced the severity of radiation-induced oral mucositis. Preclinical studies have demonstrated protective effects on skin, intestinal mucosa, and lung epithelium when KGF is administered before irradiation Farrell et al. (1999)1097-0215(19990924)83:1%3C105::aid-ijc19%3E3.0.co;2-y).

Safety Profile

Palifermin has been extensively evaluated in clinical trials with a well-characterized safety profile. The most common adverse effects include dysgeusia (taste alteration), tongue thickening, tongue discoloration, oral/perioral dysesthesia, skin rash, pruritus, erythema, and edema. These effects are generally mild to moderate, transient, and resolve within days of discontinuation. Because KGF acts exclusively on FGFR2-IIIb-expressing epithelial cells, it does not stimulate fibroblast or endothelial proliferation, reducing fibrotic and angiogenic risks. However, theoretical concerns exist regarding stimulation of FGFR2-IIIb-expressing tumors; palifermin is contraindicated in patients with known FGFR2-IIIb-expressing malignancies. Long-term safety surveillance has not identified increased cancer incidence in treated patients. Topical cosmetic formulations use KGF at concentrations far below therapeutic doses and have not been associated with significant adverse effects.

Gastrointestinal Protection

KGF exerts protective effects on gastrointestinal epithelium, which also expresses FGFR2-IIIb. Preclinical studies have demonstrated that KGF pretreatment reduces chemotherapy-induced intestinal mucositis, radiation enteritis, and inflammatory bowel disease severity. KGF promotes proliferation of intestinal crypt stem cells, thickens the mucosal barrier, and increases mucus production. These findings suggest potential applications beyond oral mucositis, though clinical development has focused on the FDA-approved indication Houchen et al. (1999).

Lung Epithelial Protection

FGFR2-IIIb is expressed on alveolar type II pneumocytes, and KGF stimulates surfactant production, alveolar epithelial repair, and edema clearance. Preclinical research has explored KGF for acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and ventilator-induced lung injury. Intravenous palifermin increased alveolar epithelial fluid clearance in human ex vivo lung perfusion models, suggesting potential for treating pulmonary edema and improving lung transplant outcomes McAuley et al. (2004).

Pharmacokinetic Profile

KGF (Keratinocyte Growth Factor) — Pharmacokinetic Curve

Intravenous (Palifermin), Topical (cosmetic)
0%25%50%75%100%0m4.5h9h13.5h18h22.5hTimeConcentration (% peak)T_max 1.8hT_1/2 4.5h
Half-life: 4.5hT_max: 1.8hDuration shown: 22.5h

Quick Start

Route
Intravenous (Palifermin), Topical (cosmetic)

Molecular Structure

Molecular Properties
Formula
Protein (~19 kDa)
CAS
162394-19-6 (Palifermin)

Research Protocols

oral

The recombinant form, palifermin (Kepivance), is FDA-approved for the prevention of severe oral mucositis in hematologic malignancy patients undergoing myeloablative therapy and stem cell transplantation. Research Mucositis Prevention (FDA-Approved) Palifermin is FDA-approved for prevention of seve

topical

In animal models, topical KGF application has demonstrated accelerated closure of full-thickness wounds, improved epithelial barrier function, and enhanced tensile strength of healed tissue. Topical and injectable KGF formulations have shown promise in stimulating hair growth in androgenetic alopeci

intravenous Injection

Intravenous palifermin increased alveolar epithelial fluid clearance in human ex vivo lung perfusion models, suggesting potential for treating pulmonary edema and improving lung transplant outcomes [McAuley et al. Clinical (palifermin) formulations are administered intravenously as a lyophilized pow

GoalDoseFrequency
General Research Protocol60 mcgPer protocol

What to Expect

What to Expect

Onset

Effects begin within hours of administration based on half-life of ~4.5 hours (Palifermin IV)

Days 1-3

In pivotal clinical trials, palifermin reduced the incidence of WHO grade 3-4 oral mucositis from 98% to 63% and shortened the duration of severe...

Daily Use

Due to short half-life (~4.5 hours (Palifermin IV)), effects are expected per-dose; consistent daily administration maintains therapeutic levels

Study Observations

In pivotal clinical trials, palifermin reduced the incidence of WHO grade 3-4 oral mucositis from 98% to 63% and shortened the duration of severe...

Ongoing

Regular administration schedule required; effects are dose-dependent and do not persist between doses

Quality Indicators

What to look for

  • Human clinical trials conducted
  • Well-established safety profile
  • Multiple peer-reviewed studies available

Frequently Asked Questions

References (11)

  1. [17]
  2. [8]
    Finch & Rubin *J J. Cell. Biochem. (2004)
  3. [9]
    Spielberger et al *N N. Engl. J. Med. (2004)
  4. [10]
    Werner *Cytokine Growth Factor Rev.*, 9(2), 153-165 Cytokine Growth Factor Rev. (1998)
  5. [11]
    Danilenko et al *Am Am. J. Pathol. (1995)
  6. [12]
    Farrell et al *Int Int. J. Cancer (1999)
  7. [13]
    Rubin et al *Proc Proc. Natl. Acad. Sci. USA (1989)
  8. [14]
    Braun et al *Cytokine Growth Factor Rev.*, 15(2-3), 91-102 Cytokine Growth Factor Rev. (2004)
  9. [15]
  10. [16]
  11. [18]
Updated 2026-03-087 citationsSources: peptide-wiki-mdx, peptide-wiki-mdx-v2

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