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Pipeline

10 programs, one engine.

Seven cosmetic actives, two drug assets, and one dual-track program — each a novel, patent-filed approach to a defined driver of skin aging.

7
Cosmetic
2
Drug
1
Dual-track
10
Patents filed
01Cosmetic
KEAP1 inhibitor
Switches on skin's own antioxidant defense (NRF2)
vs Vit C/E, niacinamide22 seq
02Cosmetic
14-3-3σ / stratifin modulator
Blocks a signal that degrades collagen (MMP-1)
vs Retinoids12 seq
03Cosmetic
Copper (ATCUN/GHK)
Collagen-boosting copper, released only in aged skin
vs GHK-Cu peptides10 seq + prodrugs
04Cosmetic
Methylglyoxal scavenger
Traps the sugars that stiffen & yellow collagen
vs Carnosine7 seq
05Cosmetic
Radical-Scavenger
Antioxidant peptides hardened against self-oxidation
vs Carnosine, Vit C/E11 seq
06Cosmetic
Multi-active
Multi-active with designed synergy
vs Multi-active serums10 seq
07Cosmetic
MMP-12 inhibitor
Stops an enzyme that destroys elastin
vs Retinoids, MMP appr.10 compounds
08Drug
GATA4 degrader
Quiets senescent-cell inflammation (senomorphic)
vs Senomorphicsdefensive filing
09Drug
BCL-xL senolytic
Selectively clears senescent skin cells
vs Systemic senolyticsfiled
10Dual
KLK5 inhibitor
Calms reactive skin by reining in barrier-degrading KLK5
vs Azelaic acid, soothersfiled

Program 01 · KEAP1 inhibitor

Turn on the skin's own defense.

Skin has a built-in antioxidant program (NRF2) held "off" by a protein called KEAP1. Our cyclic peptides release the brake, so skin makes its own protective enzymes.

Cosmetic22-sequence provisional · lead chemotypes + SAR + permeability variants
On the marketTopical antioxidants (Vit C/E), niacinamide, plant NRF2 boosters — indirect, low-potency, unstable.
Our designDirectly targets the KEAP1 switch with novel cyclic peptides engineered to avoid the natural degron motif — for selectivity and clean IP white space.

Program 02 · 14-3-3σ / stratifin modulator

Protect collagen at the source.

A secreted signal called stratifin tells skin cells to make MMP-1, the enzyme that chews up collagen. Our peptide is designed to intercept that signal.

Cosmetic12-sequence provisional · monovalent + bivalent + phosphomimetic designs
On the marketRetinoids and generic peptides reduce MMPs broadly and indirectly.
Our designFirst-in-class approach aimed at the specific stratifin → MMP-1 axis — a literature-verified mechanism met with a purpose-built binder.

Program 03 · Copper (ATCUN/GHK)

The smart copper peptide.

Copper peptides boost collagen — but copper everywhere can harm. Ours is a prodrug that releases active copper only in the high-oxidative-stress environment of aged skin, with a redox-silenced anchor.

Cosmetic10 peptide sequences + 6 prodrug designs
On the marketGHK-Cu copper peptides and Matrixyl — effective but decades-old, off-patent, commodity, and "always-on."
Our designTargeted release where damage is occurring + antioxidant copper handling = differentiated, patentable chemistry vs. the generic tripeptide.

Program 04 · Methylglyoxal scavenger

Stop sugar from stiffening skin.

Blood-sugar byproducts (methylglyoxal) cross-link collagen — making skin stiff, dull, and yellow (glycation / "AGEs"). Our cyclic peptides trap those reactive sugars before they hit collagen.

Cosmetic7-sequence provisional · Arg-, Lys-, and ornithine-based leads
On the marketCarnosine is the standard antiglycation active — but it's a small dipeptide rapidly broken down by carnosinase.
Our designCyclic, carnosinase-resistant histidine traps engineered for greater stability and trapping potency than carnosine.

Program 05 · Radical-Scavenger

Antioxidants that don't backfire.

Quench damaging free radicals with His / Tyr antioxidant peptides — engineered so they don't turn pro-oxidant themselves, a common failure of ordinary antioxidants.

Cosmetic11-sequence provisional · canonical + hardened-Tyr analogs
On the marketCarnosine, Vitamin C/E, ergothioneine — effective but can degrade or generate radicals under stress.
Our design"Oxidation-hardened" chemistry (ortho-blocked tyrosine) tuned by QM modeling to resist self-oxidation — a defensible twist on a crowded category.

Program 06 · Multi-active

Synergy by design, not by blending.

A layered active hitting glycation + antioxidant defense + copper/redox at once — exploiting a designed synergy: switching on NRF2 (P1) induces the cell's own anti-glycation enzyme (GLO1), amplifying P4.

Cosmetic10-sequence provisional · synergy to be shown in 3-D skin models
On the market"Multi-active" anti-aging serums — usually arbitrary blends with no mechanistic rationale.
Our designComponents chosen to reinforce one another mechanistically — a coherent system, not a kitchen-sink mix.

Program 07 · MMP-12 inhibitor

Preserve elastin, preserve firmness.

MMP-12 is an enzyme that destroys elastin — the fiber behind firmness and snap. Our phosphinic pseudopeptides are designed to inhibit it selectively by filling its deep specificity pocket.

Cosmetic10 lead compounds · chemical-structure filing
On the marketRetinoids and broad anti-MMP approaches. Note: DSM holds related phosphinic-MMP-12 cosmetic IP — our edge rests on distinct compound structures.
Our designDeep-pocket selectivity for MMP-12 vs. shallow housekeeping MMPs — designed to avoid broad-inhibition liabilities.

Program 08 · GATA4 degrader

Quiet senescent-cell inflammation.

Senescent ("zombie") cells drive inflammaging via a master switch, GATA4. Our targeted degrader (PROTAC) is designed to remove GATA4 and quiet the inflammatory secretome (SASP) — a senomorphic mechanism.

Drug · earliest-stageDefensive IP-lock · an Rx opportunity · candidly our least-validated program
On the marketSystemic senolytics and emerging topical senotherapeutics (e.g. OneSkin's OS-01 peptide).
Our designPrecise targeted degradation of a senescence master-regulator — and no GATA4 degrader exists today (genuine new-target white space).

Program 09 · BCL-xL senolytic

Our first true senolytic.

Senescent skin cells survive by leaning on BCL-xL, a survival protein. Our de novo cyclic peptide is designed to selectively engage BCL-xL — the basis for a first-in-class, topically delivered senolytic that clears those cells.

Drug · pre-wet-labProvisional filed · clean composition-of-matter FTO read
On the marketToday's senescence products are non-specific or repurposed; the leading branded entrant isn't a true cell-clearing agent. Systemic senolytics carry dose-limiting toxicity.
Our designEngages BCL-xL in preference to its relatives (BCL-2, MCL-1) in two independent computational methods — the relatives whose inhibition drives senolytic-drug toxicity. A defined variant family surrounds the lead.

Program 10 · KLK5 inhibitor

Calm for reactive skin.

Sensitive, reactive skin is driven by an over-active barrier protease, KLK5, that breaks down the skin barrier and sparks inflammation. Our designed inhibitor reins in KLK5 to calm reactivity at its source.

Dual-track · pre-wet-labProvisional filed · cosmetic active + Rx candidate
On the marketSensitive-skin products mostly soothe symptoms — they don't target the protease driving barrier breakdown and flare-ups.
Our designA designed KLK5 inhibitor — a dual-track asset: a cosmetic active for sensitive skin and a drug candidate for rosacea & barrier-disease (Netherton-type) indications.

IP position

White space, locked.

  • Composition & methods. Covers composition-of-matter (novel sequences / structures) and methods of use.
  • Priority secured. First-inventor-to-file priority on filing; runway to non-provisional / PCT.
  • True white space. Chemical matter is distinct from the incumbents' — we file where the old actives don't reach.
10

U.S. provisional patents filed

Each a separate application across the ten programs — composition-of-matter and methods of use.

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