FLNA-Binding Compound Targets pS2152 Filamin A for Cancer Therapy

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Solution Overview

Problem

Cancer cells exhibit elevated levels of phosphorylated proteins such as mTOR, Akt, ERK2, and serine2152-phosphorylated filamin A (pS2152-FLNA), which are not effectively regulated, leading to uncontrolled growth and survival signals, while existing therapies struggle to target these specific pathways effectively.

Innovation Solution

A method involving the use of an FLNA-binding compound that binds to the pentapeptide sequence of FLNA, reducing the levels of pS2152-FLNA and associated phosphorylated proteins, thereby inhibiting cancer cell growth by normalizing the phosphatase activity and restoring regulatory control over PI3K/Akt and mTOR pathways.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If existing therapies are used to target phosphorylated proteins in cancer cells, then cancer cell growth is inhibited, but the ability to specifically distinguish cancer cells from non-cancerous cells is insufficient

Engineering Contradiction:
Improvespecificity of cancer cell targetingVSAvoidregulatory control over phosphorylation pathways
Core Design Contradiction:
ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent applies local quality by targeting a specific phosphorylation site (serine 2152) on the FLNA protein rather than general phosphorylation pathways. This localized targeting approach allows the compound to specifically affect cancer cells with abnormal phosphorylation at this site while sparing normal cells, thereby improving specificity without compromising pathway regulation

Inventive Principle:
Principle #3Local quality

Solution Approach 2:

The patent utilizes parameter changes by detecting and targeting altered phosphorylation levels at serine 2152 of FLNA in cancer cells. The method identifies cancer cells based on this specific phosphorylation parameter and uses compounds that modify this parameter, enabling selective inhibition of cancer cell growth while maintaining normal cellular function in non-cancerous cells

Inventive Principle:
Principle #35Parameter changes

2Productivity

If broad-spectrum kinase inhibitors are used to block phosphorylation pathways, then cancer cell proliferation is reduced, but normal cellular signaling is also disrupted

Engineering Contradiction:
Improveinhibition of cancer cell proliferationVSAvoidselectivity between cancer and non-cancerous cells
Core Design Contradiction:
ProductivityVSReliability

Solution Approach 1:

The patent applies segmentation by dividing the broad phosphorylation pathway into specific segments, focusing on the FLNA protein and its serine 2152 phosphorylation site. This segmentation allows targeted inhibition of cancer cell proliferation through a specific molecular segment rather than broad-spectrum inhibition, thereby maintaining selectivity between cancer and non-cancerous cells

Inventive Principle:
Principle #1Segmentation

Solution Approach 2:

The patent uses FLNA as an intermediary target between the phosphorylation pathways and cancer cell proliferation. By targeting FLNA phosphorylation specifically at serine 2152, the compound acts as a selective mediator that interrupts cancer cell growth signals without disrupting normal cellular signaling in non-cancerous cells

Inventive Principle:
Principle #24Intermediary (Mediator)

Applied Scientific Principles

This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.

Function Achieved in This Case

The approach effectively reduces cancer cell proliferation by normalizing the levels of phosphorylated proteins, specifically targeting cancer cells while sparing non-cancerous cells, thereby inhibiting tumor growth and metastasis.

Implementation Method 1

contacting cancer cells with an FLNA-binding effective amount of a compound or a pharmaceutically acceptable salt thereof that binds to the pentapeptide of FLNA

Methodology Applied
Scientific EffectMolecular binding: Absorption (physical)

Implementation Method 2

restoring regulatory control over PI3K/Akt and mTOR pathways

Methodology Applied
Scientific EffectPhosphatase activity: Enzyme

Implementation Method 3

Phosphorylation of a protein involves the enzymatically mediated addition of a phosphate group

Methodology Applied
Scientific EffectPhosphorylation:

Data Source

PatentEP3054956B1Method for inhibiting growth of cancer cells
Publication Date: 2020.08.26 PAIN THERAPEUTICS INC
  • EP3054956B1 patent drawingFigure 1~1B
  • EP3054956B1 patent drawingFigure 1C
  • EP3054956B1 patent drawingFigure 1D~1E

AI summary

1 A method of inhibiting the growth of cancer cells is disclosed in which cancer cells that contain an enhanced amount relative to non-cancerous cells of one or more of phosphorylated mTOR, Aktl, ERK2 and serine2152-phosphorylated filamin A are contacted with an FLNA-binding effective amount of a compound or a pharmaceutically acceptable salt thereof that binds to the pentapeptide of filamin A (FLNA) of SEQ ID NO: 1 and exhibits at least about 60 percent of the FITC- labeled naloxone binding amount when present at a 10 μΜ concentration and using unlabeled naloxone as the control inhibitor at the same concentration. A compound that binds to the FLNA pentapeptide preferably also contains at least four of the six pharmacophores of Figs. 19-24.