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yellowpigment.com · Confidential · 2026
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Seed Round · Confidential · 2026
Turning a protective
human phenotype
into medicine.
First-in-class therapeutics for inflammatory and metabolic disease, built on the biology of Gilbert syndrome.
Human genetics-inspired drug discovery · Biliverdin-ester prodrug platform
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The Opportunity

Major inflammatory and metabolic diseases
remain poorly served.

Many chronic conditions still lack therapies that are both mechanistically differentiated and suitable for durable, broad disease modification.

Inflammatory Disease
Chronic inflammation at scale

Anti-phospholipid syndrome (APS) remains without FDA-approved disease-modifying therapy beyond anticoagulation

Systemic inflammatory conditions affect tens of millions globally, with significant morbidity and treatment gaps

Existing treatments target downstream pathways — few address the underlying oxidative and inflammatory biology

Metabolic Disease
Metabolic dysfunction is epidemic

Obesity, metabolic syndrome, and cardiometabolic risk affect over a billion people globally

Inflammatory and metabolic dysfunction are tightly linked — driven by shared oxidative stress pathways

Chronic low-grade inflammation ("inflammaging") is a central driver of age-related functional decline.

There is a better target hiding in human biology itself.
The Opportunity

Gilbert syndrome is a natural experiment
in protective biology.

~5–10% of people carry Gilbert syndrome — mildly elevated unconjugated bilirubin via UGT1A1 variation. Epidemiological data consistently shows protection across major disease domains.

−50%
All-cause mortality in Gilbert syndrome vs. age-matched population controls in large UK cohort study
Horsfall LJ et al. 2013 · n > 2,000
−60%
Coronary heart disease risk in UGT1A1*28 homozygotes vs. wildtype — Framingham Heart Study cohort
Lin JP et al. · Framingham
Lower BMI & fat mass
Gilbert-range bilirubin associated with lower adiposity and waist circumference, especially in adults ≥ 35 years
Seyed Khoei N et al. 2018 · Free Radic Biol Med
Inflammatory Link
Lower bilirubin tracks with elevated APS inflammatory burden — elevated BR may confer protection in autoimmune states
Multiple cohort studies
Key Insight Nature has already run the experiment. Mild bilirubin elevation appears consistently protective — across mortality, cardiovascular, metabolic, and inflammatory domains.
The Science

A validated human signal can be
translated into medicine.

The bilirubin pathway offers a translational bridge from human genetics to pharmacology — with a clear molecular target and an understood mechanism.

Precursor
Heme
HO-1 / HO-2
Intermediate
Biliverdin
BLVRA / BLVRB
⭑ Therapeutic Target
Bilirubin
⚑ Gilbert window
UGT1A1
↓ in Gilbert
Excreted
BR-Glucuronide
Bilirubin Concentration by Clinical State Plasma bilirubin (µM)
Normal
★ YPT Window
CN-II
CN-I
0
17
85
100
350
900
µM →
Normal
3.4 – 17 µM
Gilbert Syndrome ★ YPT Window
17 – 85 µM
Crigler-Najjar II
100 – 350 µM
Crigler-Najjar I
350 – 900 µM
The goal is not hyperbilirubinemia — it is controlled access to the Gilbert protective window.
The Science

Why bilirubin has not yet become
a practical drug.

The therapeutic signal is real. But bilirubin itself has been difficult to translate into a scalable, orally delivered medicine.

01 — Signal
Compelling biology
Strong epidemiological evidence across mortality, cardiovascular, metabolic, and inflammatory disease. Multiple mechanisms. Clear human phenotype. The biology works.
Validated in humans
→
02 — Problem
Delivery bottleneck
Bilirubin itself is chemically difficult. Most published attempts use injectable, infusion, or nanoparticle approaches — limiting utility for chronic disease.
Poor aqueous solubility
Chemical instability
Hard formulation
Rapid degradation by gut microbiome
→
03 — Opportunity
Oral prodrug strategy
A drug design strategy that masks the problematic chemical features of bilirubin — while preserving access to its biology. Delivered orally. Suitable for chronic use.
YPT's approach
The challenge has not been whether bilirubin biology matters. The challenge has been making it druggable.
Platform

Yellow Pigment is building
biliverdin-ester prodrugs.

Biliverdin-esters are a practical drug design strategy to access bilirubin biology in a tractable, developable format — suitable for oral delivery and chronic use.

BV-Ester
Prodrug
Oral dose
GI lumen
Esterase
Biliverdin
BV
Absorbed
Systemic
BLVRA/B
Bilirubin
BR
Active
Pharmacology
UGT1A1
Therapeutic
Effect
Gilbert-range
biology
Improved absorption
Ester groups increase lipophilicity, enabling passive GI uptake
Endogenous activation
Esterases regenerate BV → BLVRA/B converts to BR
Better CMC profile
Improved formulation path vs. bilirubin free acid
IP-protected space
Ester design creates proprietary composition-of-matter opportunity
A chemistry strategy designed for druggability, oral delivery, and mechanistic relevance.
Platform

Bilirubin biology acts across metabolism,
inflammation, and tissue protection.

This is a pleiotropic mechanism. One biology with multiple pharmacological entry points across major disease categories.

01
PPARα Modulation
Bilirubin acts as an endogenous PPARα ligand, activating fatty acid oxidation and regulating lipid homeostasis — the mechanistic basis for metabolic protection in Gilbert individuals.
Metabolic axis
02
Lipophilic Antioxidant
BR intercepts peroxyl radicals in lipid membranes — a compartment inaccessible to water-soluble antioxidants. The BV → BR → BV redox cycle amplifies capacity beyond stoichiometric ratios.
Oxidative stress
03
BLVRA Signaling
Biliverdin reductase A is a dual-function kinase. Beyond BV reduction, it modulates insulin receptor signaling (IRS-1/PI3K) and NFκB — placing it centrally in metabolic and inflammatory control.
Signaling axis
04
Microbial Modulation
BV and BR exhibit anti-viral and anti-bacterial activity at epithelial barriers, supporting immune homeostasis. Emerging evidence links Gilbert-range BR to favourable host-microbial interaction profiles.
Host–microbiome axis
One biology. Multiple therapeutic entry points across metabolic, inflammatory, and tissue-repair disease. 5–10% global Gilbert carrier rate · 4 mechanisms · 3 programs
Platform

Early evidence supports
platform plausibility.

Published and internal data support that biliverdin-ester constructs can improve membrane permeability and convert through the intended biological pathway.

Published Precedent
BV dimethyl ester (BV-Me₂) demonstrates improved membrane passage versus unmodified biliverdin in published permeability studies
BV-Me₂ is a substrate for serum and cellular esterases in vitro and in vivo, supporting the bioactivation mechanism
Epidemiological evidence across four independent study cohorts confirms the human protective phenotype
Internal Readouts
Extracellular BV-to-BR conversion confirmed in monocyte cell culture, demonstrating biologically relevant conversion
BLVRA knockout slows BV-to-BR conversion, confirming enzymatic mechanism and pathway specificity
HPLC, fluorescence (iRFP/eUnaG) and permeability assays developed to support compound screening and lead selection
The platform has an early mechanistic and translational signal — not just a theoretical idea.
Pipeline

Lead program: APS as the
first clinical wedge.

APS is an attractive initial indication — strongly connected to inflammatory and oxidative stress biology, with a focused development path and a clear bridge to larger markets.

Lead Program
Anti-Phospholipid Syndrome (APS)
A systemic autoimmune condition characterized by thrombosis, inflammatory burden, and elevated oxidative stress — with no approved disease-modifying therapy beyond anticoagulation.
Orphan potential Focused entry
  • Human data in APS links lower bilirubin with higher inflammatory burden — direct mechanistic relevance
  • Mechanism aligns with anti-inflammatory and cytoprotective biology of the BV-ester platform
  • Small, focused indication with a clear regulatory path vs. launching directly into broad metabolic markets
Expansion pathway
→
Cardiometabolic
PPARα + cardiovascular protection · post-APS credibility drives BD opportunity
→
Metabolic / Obesity
GLP-1 adjunct positioning · PPARα axis · large addressable market
→
Broader Inflammatory
Tissue repair, gut-liver axis, and oxidative stress conditions
Start focused. Success in APS creates a highly credible bridge into larger inflammatory and cardiometabolic indications.
Pipeline

One engine,
multiple programs.

A single chemistry and biology platform generates multiple disease programs over time. Shared infrastructure, cross-applicable learnings, expanding optionality.

Lead Program · Now
Inflammatory / APS
APS as focused first indication — clear mechanism and development path
BV-Me₂ as lead compound in in vitro and in vivo cascade
Human data directly supports mechanistic hypothesis
Orphan potential with bridge to cardiometabolic market
Expansion 1 · Post-Seed
Metabolic / Obesity
PPARα modulation — same mechanism, metabolic indication
GLP-1 adjunct positioning for combination use
Epidemiological data supports: Gilbert = lower BMI, better adiposity
Large addressable market with clear unmet need beyond incretin therapy
Expansion 2 · Series A
Inflammatory & Tissue Repair
Broader oxidative and inflammatory disease settings
Cross-applicable screening, tox, and translational learnings from lead programs
Candidate-specific optimization by indication using HTS library
Not a single-asset story — but we execute like one at the start.
Pipeline

A capital-efficient path to
candidate nomination.

The next phase moves from concept to validated lead candidate through a staged screening and preclinical workflow — with clear go/no-go gates at each step.

1
Library Design & CRO Synthesis
Rational design of BV-ester variants with AI/ML-guided prioritisation. CRO synthesis of initial 20–40 compound library.
4–6 mo
2
In Vitro Screening Campaign
Human serum esterase activity, membrane permeability assays (HepG2 and Caco-2), PPARα reporter, intracellular and extracellular BLVRA/BLVRB activity, bilirubin secretion activity.
Milestone 1
3–6 mo
3
In Vivo Proof-of-Concept
Mouse APS model (MRL/lpr genetic model and aPL antibody induction).
Milestone 2
6–12 mo
4
Non-GLP NHP PK/PD and Safety
Intra-animal dose escalation study to achieve target bilirubin range (50–100 μM) and assess safety before IIT or IND-enabling studies. IP filing — composition of matter + method of use. Series A fundraise position.
Milestone 3
1–6 mo
This seed round converts a compelling biological thesis into a de-risked drug program ready for Series A.
Market

Targeting large,
chronic disease markets.

Yellow Pigment is pursuing an oral therapeutic platform positioned at the intersection of two of the largest and most persistent disease categories in medicine: autoimmune / inflammatory disease and metabolic disease.

Autoimmune & Inflammatory Disease
$100B+
Annual global market
Large, chronic, high-burden indications with continued need for differentiated mechanisms.
Metabolic Disease
>1B
Patients worldwide
Massive patient scale with growing demand for durable therapies targeting core disease biology.
Economically Favorable Drug Profile
Chronic daily oral therapy
Broad patient populations. Long-term treatment duration. Favorable commercial economics for an oral, once-daily format.
Platform Expansion Path
One engine, multiple indications
Autoimmune → Metabolic → Dermatology → Longevity. One core biological engine with the potential to expand across multiple chronic disease settings over time.
Opportunity to develop a scalable oral therapy addressing major drivers of chronic disease, including obesity and inflammaging.
Market

Limited direct competition —
strong biological validation.

The biology is increasingly validated, but the field remains open when it comes to building a chronic, oral therapy designed to safely recreate the protective bilirubin phenotype.

01 — Existing Approaches
Direct Bilirubin Therapeutics
External validation of the biology — but in a format that limits utility for chronic disease.
Bilix / BRIXELLE platform — PEGylated bilirubin, i.v., early clinical
Focused primarily on acute inflammatory indications
No approved or clinical-stage oral bilirubin-elevating therapy
02 — Unmet Need
Gap in the Field
The major unmet need remains a practical format for long-term use in chronic disease.
No approved or clinical-stage therapies designed to safely elevate bilirubin for chronic disease
i.v. and nanoparticle formats not suited for daily, long-duration administration
Oral prodrug chemistry not pursued by existing players
03 — Yellow Pigment
First-in-class oral approach
Pharmacologically recreating the Gilbert protective phenotype — designed for daily, chronic use.
Oral BV-ester prodrug platform — unique chemistry approach
Designed for chronic disease settings where duration and daily dosing matter
Human genetics-validated target with Gilbert syndrome as natural proof of concept
Existing field
i.v. · acute · nanoparticle · early clinical
Yellow Pigment
oral · chronic · prodrug · daily dosing
Strong external validation of the biology — with a clear gap around oral chronic-disease therapeutics.
Why Yellow Pigment

Defensibility comes from biology,
chemistry, and execution.

Yellow Pigment combines a differentiated human biology insight with a tractable prodrug chemistry strategy and a focused development plan — across three reinforcing pillars.

I
Human Biology Insight
A hypothesis grounded in one of the most replicated protective phenotypes in human genetics — not a target identified from cell lines or animal models alone.
Human genetics-validated target
Multiple independent cohort studies
Pleiotropic mechanism across disease areas
II
Chemistry Platform
Biliverdin-ester design creates a proprietary optimization space. The prodrug strategy solves the formulation and delivery problem that has blocked prior bilirubin approaches.
BV-ester design library (40+ compounds)
Composition-of-matter IP opportunity
Better CMC profile vs. bilirubin free acid
III
Development Engine
A staged screening and preclinical workflow built to move efficiently from compound library to validated candidate — with shared infrastructure across programs.
In vitro screening: permeability + esterase + bioactivity
Cross-applicable tox and translational learnings
Capital-efficient path to Series A
A differentiated insight, a tractable chemistry strategy, and a focused path to candidate nomination.
Team & The Ask

Experienced founders raising seed capital
to reach a major inflection point.

Nikola Ivica
Nikola Ivica, PhD
Chief Scientific Officer
MIT PhD · Harvard BA. Deep expertise in heme metabolism, bilirubin biology, and therapeutic platform design. Scientific founder of the BV-ester hypothesis.
Ivan Posavec
Ivan Posavec
Chief Executive Officer
Harvard BA. Repeat biotech CEO with early-stage company building and financing experience across multiple therapeutic areas.
Luka Babić
Luka Babić
Chief Operating Officer
Harvard BA. Exited founder and operator focused on execution systems for complex ventures. Drives operational rigour across the platform build.
Seed Round
$1.3M
SAFE · 18-month runway
Synthesize and screen initial BV-ester library (40+ compounds)
Generate in vitro and in vivo proof-of-concept (APS + metabolic models)
Advance top candidates through early NHP tox work
Support IP filing — composition of matter + method of use
Goal: Nominate a Yellow Pigment development candidate and position the company for Series A financing or strategic partnering with a biopharmaceutical partner.
Key milestones funded
✓ Library design + CRO synthesis
✓ In vitro screening cascade
✓ In vivo efficacy (mouse APS + DIO)
✓ IP portfolio filing
→ Development candidate nomination