Preclinical (cell/animal)NeuroprotectionNot a peptide — synthetic research compound

CNB-001

Synthetic pyrazole-curcumin derivative – not a peptide, small molecule · Pyrazol-Curcumin-Derivat CNB-001 · CAS no. 1019110-87-2

CNB-001 is a synthetic, non-peptide small molecule – a pyrazole derivative of the spice compound curcumin. It was developed in the laboratory of David Schubert at the Salk Institute to combine the antioxidant and anti-inflammatory properties of curcumin with improved stability and potency. In cell and animal experiments, CNB-001 is described as broadly neuroprotective and neurotrophic. It is at the same time an important structural-chemical intermediate step on the path from curcumin to the better-known compound J-147. All the evidence comes from preclinical in-vitro and animal models; there are no clinical trials in humans, and CNB-001 is not approved as a medicinal product anywhere.

Machine-assisted translation. The German original is the authoritative version.

At a glance

Substance class: Synthetic pyrazole derivative of curcumin (non-peptide small molecule)
Origin: Schubert laboratory, Salk Institute (Liu et al., 2008)
CAS number: 1019110-87-2
Relationship to J-147: Structural-chemical precursor/relative on the path to J-147
Reported direction of action: Neuroprotective, neurotrophic, antioxidant, anti-inflammatory (preclinical)
Models studied: Stroke (ischemia), traumatic brain injury, neurotoxicity and memory models – cells/animals only
Development status: Purely preclinical – no clinical trials in humans

Origin & development

CNB-001 originated in the research group of David Schubert at the Salk Institute (La Jolla, USA). Liu and colleagues synthesized a series of hybrid molecules from curcumin (a plant polyphenol) and cyclohexyl-bisphenol A (a compound with neurotrophic activity). CNB-001 proved to be the most promising compound: it showed markedly improved metabolic stability compared with curcumin and was neuroprotective in several neurotoxicity assays in which curcumin itself was ineffective.

CNB-001 is also the structural reference point for the later, better-known compound J-147: from numerous CNB-001 derivatives a more potent molecule emerged – J-147. Its structure is derived from the presumed bioactive fragment of CNB-001. The development line is therefore: curcumin → CNB-001 → J-147.

Reported mechanisms of action

In the preclinical literature, CNB-001 is described as a "pleiotropic" compound – that is, a molecule that is said to act on several signaling pathways simultaneously rather than addressing a single target protein. According to the developers, it combines the antioxidant and anti-inflammatory properties of curcumin with neurotrophic effects. In cell models of stroke, the protection is attributed to the preservation of the PI3K-Akt signaling pathway, the maintenance of cellular ATP levels, as well as a modulation of calcium-calmodulin-dependent protein kinase II (CaMKII). CNB-001 is also classified as an inhibitor of 5-lipoxygenase.

Important: these mechanisms come from cell and animal experiments. Transferability to humans is not established.

Preservation of the PI3K-Akt signaling pathway and ATP levels in in-vitro stroke models
Modulation of CaMKII activity
Described inhibition of 5-lipoxygenase (anti-inflammatory)
Antioxidant action and preservation of the mitochondrial membrane potential
Described as "pleiotropic/multi-target" rather than single-target

Preclinical findings: stroke, trauma, and memory

CNB-001 has been investigated in several preclinical disease models. In models of cerebral ischemia (stroke), the Salk researchers reported an improvement of behavioral and molecular deficits. In a rabbit model of ischemic stroke, efficacy was described even with delayed administration after the event. In addition, CNB-001 was described as neuroprotective in models of traumatic brain injury as well as in neurotoxicity and memory models.

These results are encouraging, but all preclinical. Animal models of stroke reflect the complex human disease only to a limited extent; many neuroprotective candidates have failed in the past during the transition to humans.

Improved behavioral and molecular findings in animal models of ischemic stroke
Reported efficacy with delayed administration in the rabbit stroke model
Neuroprotection in models of traumatic brain injury
Protection in cell models against oxidative stress, excitotoxicity, and amyloid toxicity
All findings from cell culture and animal experiments – no confirmation in humans

Development status and context

CNB-001 is exclusively at the preclinical stage. The developers themselves describe the substance as a lead structure with a favorable safety and pharmacokinetic profile that "should be developed further." This very wording makes clear that clinical development in humans has not taken place; a continuation toward primate and clinical trials was merely named as a goal.

For a compound profile, this means: CNB-001 is a pure research substance without approval, without proven benefit or safety in humans, and without validated use. It is neither a medication nor a dietary supplement.

Status: preclinical – no registered clinical trials in humans
Designated by the developers as a lead compound
Not an approved medicinal product in any region
Benefit and safety for humans are not established

Regulatory status

General

Not approved / purely investigational

CNB-001 is not approved as a medicinal product anywhere. It is a preclinical research substance without proven benefit or safety evidence in humans.

Germany (AMG)

Not an approved medicinal product

There is no approval under medicines law. Use in humans would be permissible only within the framework of an authorized clinical trial; no such trials are known.

Sport (WADA)

Not listed by name

CNB-001 is not listed by name on the WADA prohibited list. Unapproved, purely experimental substances may, however, fall under category S0 ("non-approved substances") and would thus be prohibited in sport at all times.

Safety & context

There are no safety data from human trials – the safety profile is based exclusively on cell and animal experiments.
CNB-001 is not an approved medicinal product and not a dietary supplement; self-administration is not intended and not advisable.
Purity, identity, and composition of material offered as a "research chemical" are not quality-assured.
Long-term effects, interactions, and possible toxicity in humans are unknown.
This presentation serves scientific information purposes only and contains no dosing or usage instructions.

Frequently asked questions

Is CNB-001 a peptide?: No. CNB-001 is not a peptide but a synthetic, non-peptide small molecule – specifically a pyrazole derivative of the natural compound curcumin.
What does CNB-001 have to do with J-147?: CNB-001 is the chemical precursor or reference molecule on the path to J-147. From numerous CNB-001 derivatives, the more potent J-147 emerged; the development line runs from curcumin via CNB-001 to J-147.
Are there clinical trials or an approval for CNB-001?: No. CNB-001 has so far been investigated only preclinically (in cells and animal models). There are no known clinical trials in humans and no approval under medicines law in any region.

Sources

This profile is for information and education only. It does not replace medical advice and deliberately contains no dosing, reconstitution, usage or sourcing information.

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