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Lk2(6)a

Intervention

1 paper1 finding

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

On aging: the drug’s trials ARN judged to be about aging, of every trial that tests it for any use.

No results posted: trials that ended more than a year ago with no results on ClinicalTrials.gov and no paper in ARN’s record.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

  • 1 lab in 1 country
  • Funders: Key Research Project of Liaoning and 1 more
  • Model organisms1

Outcomes

1

Inflammation

downin mouse cells1

1 study

  1. Lk2(6)a decreases inflammation in mouse cells.

    “Temporin-1CEa and LK2(6)A(L) inhibited the release of pro-inflammatory mediators by downregulating the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways.”

    Cellsin LPS-stimulated BV2 microglial cells

    Temporin-1CEa and its Analog LK2(6)A(L) Confer Neuroprotective Effects in Parkinson's Disease Model by Attenuating Neuroinflammation Via the NF-κB and MAPK Signaling Pathways

    Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology6 Oct 2025

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