Certificate of Analysis

1441 in stock

Quantity Price / Per Vial
1 – 3 $76.00
4 – 7 $70.00
8+ $65.00

KPV 10MG

$76.00

Certified-Pep only sells U.S.-made peptides and products.

Key Features
  • Made in the USA
  • Batch tested at a verifiable U.S. laboratory for identity, content and purity
  • Screened for endotoxins, heavy metals and sterility
  • Rigorous quality testing on every batch
  • All products are delivered in lyophilized powder form
  • For laboratory and research use only
  • PURITY: 99%+
  • CAS: 112965-21-6
  • FORM: LYOPHILIZED POWDER
  • DOSAGE: 10 MG
  • PURITY: 99%+

Description

KPV 10MG
SKU CP_KPV_10MG_3ML_VIAL
CATEGORY Lyophilized Peptide
CAS 112965-21-6
VIAL SIZE 3 mL
FORM LYOPHILIZED POWDER
MOLECULAR WEIGHT 384.48 g/mol
SEQUENCE Ac-Lys-Pro-Val-NH2
MOLECULAR FORMULA C17H32N6O4
ITEM ID 11689

KPV 10MG provides KPV as lyophilized powder in a 3 mL vial.

Research Context

In Vitro: Keratinocyte Model – Fine Particulate Matter Exposure

In human HaCaT keratinocytes exposed to PM10, KPV was examined for its effects on reactive oxygen species (ROS) production, MAPK/NF-κB signaling, and markers of apoptosis. KPV was associated with attenuation of ROS generation and modulation of signaling intermediates including ERK, p38, and NF-κB. Changes in apoptosis-related protein expression (Bax, Bcl-2, cleaved caspase-3) and IL-1β levels were also reported. Observations were extended to a three-dimensional reconstructed skin model [Sung et al., 2025].

In Vitro: 3T3-L1 Preadipocyte Differentiation Model

In 3T3-L1 preadipocytes induced to differentiate, KPV was evaluated for effects on lipid-staining intensity and adipogenic marker expression. KPV was associated with reduced Oil Red O staining intensity and intracellular triglyceride content in a concentration-dependent manner, along with decreased expression of PPARγ and fatty acid synthase (FAS). Mechanistic analysis indicated involvement of ROS-dependent AKT/mTORC1 signaling [An et al., 2026].

In Vitro: HepG2 Hepatocyte Lipid-Loading Model

In oleic acid-treated HepG2 hepatocytes, KPV was assessed for effects on intracellular lipid accumulation and associated signaling markers. KPV was associated with reduced intracellular lipid accumulation and suppressed FAS expression, with mechanistic data pointing to modulation of ROS generation, ERK activation, and AKT/mTORC1/PPARγ phosphorylation [Lee et al., 2026].

Description

Description

KPV 10MG
SKU CP_KPV_10MG_3ML_VIAL
CATEGORY Lyophilized Peptide
CAS 112965-21-6
VIAL SIZE 3 mL
FORM LYOPHILIZED POWDER
MOLECULAR WEIGHT 384.48 g/mol
SEQUENCE Ac-Lys-Pro-Val-NH2
MOLECULAR FORMULA C17H32N6O4
ITEM ID 11689

KPV 10MG provides KPV as lyophilized powder in a 3 mL vial.

Research Context

In Vitro: Keratinocyte Model – Fine Particulate Matter Exposure

In human HaCaT keratinocytes exposed to PM10, KPV was examined for its effects on reactive oxygen species (ROS) production, MAPK/NF-κB signaling, and markers of apoptosis. KPV was associated with attenuation of ROS generation and modulation of signaling intermediates including ERK, p38, and NF-κB. Changes in apoptosis-related protein expression (Bax, Bcl-2, cleaved caspase-3) and IL-1β levels were also reported. Observations were extended to a three-dimensional reconstructed skin model [Sung et al., 2025].

In Vitro: 3T3-L1 Preadipocyte Differentiation Model

In 3T3-L1 preadipocytes induced to differentiate, KPV was evaluated for effects on lipid-staining intensity and adipogenic marker expression. KPV was associated with reduced Oil Red O staining intensity and intracellular triglyceride content in a concentration-dependent manner, along with decreased expression of PPARγ and fatty acid synthase (FAS). Mechanistic analysis indicated involvement of ROS-dependent AKT/mTORC1 signaling [An et al., 2026].

In Vitro: HepG2 Hepatocyte Lipid-Loading Model

In oleic acid-treated HepG2 hepatocytes, KPV was assessed for effects on intracellular lipid accumulation and associated signaling markers. KPV was associated with reduced intracellular lipid accumulation and suppressed FAS expression, with mechanistic data pointing to modulation of ROS generation, ERK activation, and AKT/mTORC1/PPARγ phosphorylation [Lee et al., 2026].

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