What is the half-life of GHK-Cu?

GHK-Cu has a half-life of ~1-2 hours (injectable); varies topically, which is why it's typically administered Once daily for optimal therapeutic effect.

How do I reconstitute GHK-Cu?

Add bacteriostatic water to the peptide vial slowly down the side. Typical reconstitution uses 2-3ml of water for a 5mg vial. Gently swirl, do not shake.

Healing & Recovery

Preclinical

GHK-Cu

Also known as: Copper Peptide, GHK Copper, Tripeptide-1 Copper

Overview

Key Facts

Primary Goal: A naturally occurring copper-binding tripeptide known primarily for skin rejuvenation and wound healing

A naturally occurring copper-binding tripeptide known primarily for skin rejuvenation and wound healing. GHK-Cu is included in the sleep category because gene expression studies reveal it upregulates genes involved in circadian rhythm regulation and nervous system repair. By modulating over 4,000 genes — including those governing neuroinflammation and oxidative stress — GHK-Cu may indirectly support sleep quality through systemic tissue restoration and reduced inflammatory burden. Half-Life ~1-2 hours (injectable); varies topically Typical Dose 1–3 mg Frequency Once daily Cycle Length 4-8 weeks on, 2-4 weeks off

Dosing Information

Half-Life

~1-2 hours (injectable); varies topically

Typical Dose

1–3 mg

Frequency

Once daily

Cycle Length

4-8 weeks on, 2-4 weeks off

Administration Routes:

subcutaneoustopical

Storage & Reconstitution

Unreconstituted (Powder)

Temperature2–8°C (36–46°F)

DurationUp to 3 months

Reconstituted (Mixed)

Temperature2–8°C (36–46°F)

Duration2-4 weeks

Research Summary

Preclinical

Broad Institute Connectivity Map data revealed that GHK-Cu modulates expression of 32% of human genes, including clusters associated with circadian rhythm, neuronal function, and inflammatory regulation. While not traditionally classified as a sleep peptide, its broad gene-regulatory profile supports systemic conditions conducive to restorative sleep. Dr. Loren Pickart's research demonstrated anti-inflammatory and neuroprotective effects that are mechanistically relevant to sleep quality. Clinical evidence for direct sleep improvement is indirect, based on gene expression and anti-inflammatory data rather than sleep-specific trials.