Science

Reinventing Pain Relief at
the Molecular Level

The Problem

Traditional morphine creates a twofold burden on patients: physiological (dose-limiting respiratory depression and tolerance) and social (risk of drug abuse, diversion, and stigma)

Increased drug liking and abuse liability
Increased risk of respiratory depression

MLB-001 integrates three synergistic pharmacologic mechanisms

Engineered for rapid onset, prolonged duration, and comparable efficacy at half the conventional morphine dose.

Mechanism of Action

Controlling the Pharmacokinetics of Morphine

Traditional Morphine

Traditional Morphine mechanism of action
  1. 1

    Morphine binds to mu receptor and causes excessive release of glutamate

  2. 2

    Glutamate binds to the NMDA receptor, eventually re-sensitizing the neuron and leading to more and more Morphine being needed

  3. 3

    Activation of NMDA receptors increases calcium influx, promotingneuroadaptations linked to tolerance, central sensitization, reward-related reinforcement, and abuse potential (drug liking).

MBL-001

MBL-001 mechanism of action
  1. 1

    Morphine binds to mu receptor, as before

  2. 2

    Quinidine protects Dextromethorphan from being rapidly metabolized, increasing its bioavailability more than twenty-fold

  3. 3

    Dextromethorphan binds and inactivates the NMDA receptor, blocking the vicious cycle

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Morphine

Drives potent, fast-onset analgesia.
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Dextromethorphan

Enhances and extends morphine’s analgesic window
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Quinidine

Stabilizes dextromethorphan exposure
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MindLab’s Class Effect

MindLab’s clinical development evaluates analgesic potency at 50% morphine dosing, reduced side effects, extended duration, and faster onset.

Half the Dose

Fewer Side Effects

Faster Onset

Longer Duration

Validated Proof of concept

Our goal is for a safer, longer-lasting therapeutic that maintains efficacy while reducing the pharmacologic triggers of drug abuse.