Cognitive & neuroEvidence C3 cited

CAQK

aka CAQK tetrapeptide · brain-homing peptide · Cys-Ala-Gln-Lys

Brain-injury-homing tetrapeptide targeting chondroitin sulfate proteoglycans at injury sites.

Route

Subcutaneous injection

Sequence

One-letter4 residues

CAQK

Three-letter

Cys-Ala-Gln-Lys

Read this before quoting the sequence

Linear tetrapeptide identified by in vivo phage display screening in mice with acute brain injury. Used as a homing/targeting ligand rather than as a therapeutic in its own right; the cysteine provides a thiol for conjugation to nanoparticles and cargo.

Source ↗

Mechanism of action

Four-amino-acid peptide (Cys-Ala-Gln-Lys) that homes to sites of acute brain and spinal injury by binding chondroitin sulfate proteoglycans upregulated in damaged tissue. Used as a targeting/repair-delivery peptide in research.

What the evidence actually shows

Grade C

Published EMBO Molecular Medicine 2025. Preclinical only.

Regulatory status

Status

Not an approved drug in any jurisdiction identified; a preclinical research targeting ligand. No registered human clinical trial found on ClinicalTrials.gov.

Clinical stage

Preclinical (mouse models and ex vivo human tissue only)

Source ↗

Dosing — what backs each figure

CAQK has never been given to a human. It is a four-amino-acid homing peptide used in research almost exclusively as a targeting tag conjugated to nanoparticles carrying an actual drug — a 2024 systematic review of 16 studies found none that evaluated CAQK alone therapeutically. The only free-peptide efficacy regimen published is 2.5 mg/kg/day intravenously for 7 days in rats with spinal cord injury.

PreclinicalAnimal studies — not a human dose

2.5 mg/kg once daily for 7 days, beginning 1 hour post-injury, in a C5 hemicontusion spinal cord injury model
rat (female Sprague-Dawley) · intravenous · PMID 42378652
Single dose of 0.24 mg methylprednisolone-loaded porous silicon nanoparticles conjugated to CAQK, in a lysolecithin-induced demyelination model
mouse (male) · intravenous · PMID 38107502

Animal doses do not convert to human doses by body weight alone. Route matters too — a compound dosed intraperitoneally in mice tells you little about subcutaneous use.

No established human dose

No approved label or completed human trial establishes a dosing regimen for this compound. Anything presented as a standard protocol for it — anywhere — is someone's convention rather than a finding.

Handling and storage

No compound-specific stability data exists

No stability or storage study for CAQK was located. Note that the N-terminal free cysteine thiol is chemically oxidation-prone (it is exploited for conjugation in the cited papers), but no measured stability figures are published. No compound-specific stability study (lyophilised or reconstituted) was located in a primary/regulatory source during this verification pass. Only generic synthetic-peptide handling guidance exists for this compound; no specific temperatures or durations are recorded here rather than fabricating them. General peptide handling still applies — reconstitute gently, keep it cold, keep it dark — but any specific figure you see quoted for this compound elsewhere is someone's assumption, not a measurement.

→ Reconstitution walkthrough → Reconstitution calculator

Safety

References (3)

Mann AP, et al. (2016) A peptide for targeted, systemic delivery of imaging and therapeutic compounds into acute brain injuries. ↗
Nature CommunicationsPMID 27351915DOI
Original identification of CAQK by in vivo phage display. CAQK selectively bound injured mouse and human brain tissue and, injected systemically (50 nmol of FAM-CAQK), homed to injury sites in penetrating brain injury and controlled cortical impact mouse models. The target is a proteoglycan complex including versican, tenascin-R and Hapln.
Abi-Ghanem C, et al. (2022) CAQK, a peptide associating with extracellular matrix components targets sites of demyelinating injuries. ↗
Frontiers in Cellular NeurosciencePMID 36072569DOI
Intravenously administered CAQK accumulated selectively at demyelinating lesion sites across three mouse models and was absent from healthy tissue, associating with fibrous extracellular matrix near reactive astrocytes.
Waggoner LE, et al. (2022) Porous Silicon Nanoparticles Targeted to the Extracellular Matrix for Therapeutic Protein Delivery in Traumatic Brain Injury. ↗
Bioconjugate ChemistryPMID 36017941DOI
Used CAQK-targeted porous silicon nanoparticles to deliver BDNF in traumatic brain injury, addressing BDNF's instability in blood and poor brain transport.

Data provenance

Chemistry and citations on this page were checked against primary sources on 2026-08-14. Values that could not be verified were left blank rather than filled with a plausible guess.

Could not verify
molecularFormula, molecularWeight, casNumber, pubchemCid, storage.lyophilized, storage.reconstituted, storage.lightSensitive, reconstitution.solvent, regulatory.wada

Research use only

This profile is educational reference material. It is not medical advice, not a prescription, and not an endorsement of self-administration. Compounds discussed here are research chemicals and most are not approved for human therapeutic use.

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