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From the body

PALDAN-palmitoyl-dopamine

An endogenous N-acyl dopamine, inactive at TRPV1 but able to potentiate NADA and anandamide.

Endogenous
Level of detail

C₂₄H₄₁NO₃

CAS 136181-87-8

Family
Endocannabinoid or related mediatorEndocannabinoidome
Molar mass
391.60 g/mol

Updated on

In plain terms

N-palmitoyl dopamine is a molecule the body makes itself: it joins dopamine to a very common fatty acid, palmitic acid. It has been found in mammalian nervous tissue, never in hemp. On its own it does not activate the TRPV1 sensor; its interest comes from its ability to strengthen the action of other endocannabinoid-system molecules.

Receptors and activity

Target network

TRPV1Positive allosteric modulatorInactive alone (no calcium influx in HEK293 expressing the receptor, no effect on withdrawal latency in the rat; Chu 2003). Preincubated for five minutes between 0.1 and 10 µM, it lowers the EC50 of NADA from about 90 nM to about 30 nM, potentiates anandamide (50 nM) and acts synergistically with a pH of 6.0 to 6.7 (De Petrocellis 2004)
  • Activates
  • Blocks or inhibits

The lower the cited value, the closer the target sits to PALDA: one ring per factor of 100. A target with no measured value stays on the edge.

Where these targets live

Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of PALDA.

Brain, side view
Body, front view
Blood

TRPV1TRPV1 found in 7 regions of the body

  1. Sensory gangliapresentExpressed in dorsal root ganglia1
  2. Spinal cordpresentNerve fibres in the spinal dorsal horn2
  3. CortexpresentParietal cortex neurons (layers 3 and 5)3
  4. SkinpresentWidely distributed in the skin4
  5. Blood vesselspresentPresent on dermal blood vessels4
  6. BonepresentPresent on osteoclasts5
  7. LiverpresentRNA enriched in the liver6

Map sources

  1. Cortright DN et al. The tissue distribution and functional characterization of human VR1. Biochem Biophys Res Commun, 2001 (new tab)
  2. Facer P et al. Differential expression of the capsaicin receptor TRPV1 and related novel receptors TRPV3, TRPV4 and TRPM8 in normal human tissues and changes in traumatic and diabetic neuropathy. BMC Neurol, 2007 (new tab)
  3. Mezey E et al. Distribution of mRNA for vanilloid receptor subtype 1 (VR1), and VR1-like immunoreactivity, in the central nervous system of the rat and human. Proc Natl Acad Sci U S A, 2000 (new tab)
  4. Ständer S et al. Expression of vanilloid receptor subtype 1 in cutaneous sensory nerve fibers, mast cells, and epithelial cells of appendage structures. Exp Dermatol, 2004 (new tab)
  5. Rossi F et al. The endovanilloid/endocannabinoid system in human osteoclasts: possible involvement in bone formation and resorption. Bone, 2009 (new tab)
  6. Human Protein Atlas. TRPV1 tissue expression (RNA consensus) (new tab)

Cited values

  1. TRPV1Positive allosteric modulatorno measured value cited

    Inactive alone (no calcium influx in HEK293 expressing the receptor, no effect on withdrawal latency in the rat; Chu 2003). Preincubated for five minutes between 0.1 and 10 µM, it lowers the EC50 of NADA from about 90 nM to about 30 nM, potentiates anandamide (50 nM) and acts synergistically with a pH of 6.0 to 6.7 (De Petrocellis 2004)

  2. IgE-dependent degranulation (RBL-2H3 mast cells)InhibitorIC50 = 3.5 µM · rat24 out of 100

    Yoo et al. 2013, Lipids (new tab) · beta-hexosaminidase release, RBL-2H3 cells activated by IgE complexes; IC50 2.2 µM for TNF-α; decreased phosphorylation of Syk, ERK1/2, Akt, cPLA2 and 5-LO

Bar length follows the measured value (Ki, Kd, EC50 or IC50), on one scale shared by every entry, from 100 µM to 0.1 nM. A target with no cited value has no bar.

Pharmacology

PALDA belongs to the N-acyl dopamine family, led by NADA. Unlike the latter, it does not activate the TRPV1 channel: in HEK293 cells expressing the receptor it caused no calcium influx, and in the rat it produced neither spontaneous pain behaviour nor thermal hyperalgesia (Chu 2003). Its documented activity is indirect: pre-incubated for five minutes, it lowers NADA's EC50 at TRPV1 from about 90 to about 30 nM between 0.1 and 10 µM, also potentiates anandamide at 50 nM and acts in synergy with acidic pH, behaviour described as an « entourage » effect (De Petrocellis 2004). No notable affinity has been reported for CB1 or CB2. Outside the vanilloid route, work on RBL-2H3 mast cells identifies PALDA as the most active of the N-acyl dopamines studied against IgE-complex-triggered degranulation: it inhibited the release of β-hexosaminidase (IC50 3.5 µM) and of TNF-α (IC50 2.2 µM), reduced the formation of prostaglandin E2, prostaglandin D2 and leukotriene C4, and lowered the phosphorylation of Syk, ERK1/2, Akt, cPLA2 and 5-lipoxygenase, without affecting Lyn (Yoo 2013). All of this remains confined to cells and animals: human data are entirely lacking, no clinical study exists, and the fate of the molecule given from outside has not been characterised.

Key sources.

History

Source
An endogenous mammalian lipid, absent from cannabis and from any documented plant source. PALDA was identified in bovine striatal extracts (Chu 2003), and N-acyl dopamines have been found in bovine and rat nervous tissues (De Petrocellis 2004). No tissue concentration is published for this congener.

Biosynthetic pathway

In vivo

An amide conjugation between dopamine and palmitic acid; no synthetic enzyme specific to PALDA has been characterised. For the family's lead compound NADA, two pathways are proposed: an N-acyl tyrosine processed by tyrosine hydroxylase and then by aromatic amino acid decarboxylase, or enzymatic conjugation of the fatty acid with dopamine, which requires tyrosine hydroxylase in the striatum; FAAH appears rate-limiting for NADA biosynthesis (Grabiec & Dehghani 2017).

Classification

Family, origin and source verification

Family

Endocannabinoid or related mediator › Endocannabinoidome

Verification

Every fact on this entry was checked against its primary sources on 20 October 2026.

Wikipedia (English)

No dedicated article.

References

  1. Chu et al. 2003, J Biol Chem: identification of PALDA in the bovine striatum, inactivity at VR1 (new tab)PMID 12569099
  2. De Petrocellis et al. 2004, Br J Pharmacol: actions of two saturated N-acyl-dopamines on TRPV1 channels (« entourage » effect) (new tab)PMID 15289293
  3. Yoo et al. 2013, Lipids: inhibitory effect of N-acyl-dopamines on the IgE-dependent response of RBL-2H3 cells (new tab)PMID 23377981
  4. Grabiec & Dehghani 2017, Cannabis Cannabinoid Res: NADA, endocannabinoid and endovanilloid (biosynthetic pathways of the family) (new tab)PMID 29082315
  5. Zajac et al. 2014, PLoS One: metabolism of N-acyl-dopamines, O-methylation by COMT (new tab)PMID 24465516
  6. Akimov et al. 2009, Biochemistry (Mosc): sulfation of N-acyl-dopamines in rat tissues (new tab)PMID 19645674
  7. Connor, Vaughan & Vandenberg 2010, Br J Pharmacol: N-acyl amino acids and neurotransmitter conjugates (review) (new tab)PMID 20649585
  8. PubChem CID 16759163, N-palmitoyldopamine (new tab)

Identifiers

Names

Common name
N-palmitoyl-dopamine
IUPAC name
N-[2-(3,4-dihydroxyphenyl)ethyl]hexadecanamide
Other names
N-palmitoyldopamine · N-palmitoyl dopamine · PALDA · NP-DA

Identifiers

Formula
C₂₄H₄₁NO₃
CAS
136181-87-8
PubChem CID
16759163(new tab)
InChIKey
TWJJFOWLTIEYFO-UHFFFAOYSA-N
SMILES
CCCCCCCCCCCCCCCC(=O)NCCC1=CC(=C(C=C1)O)O

Machine-readable entry (JSON)

LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.