Direct answer
What is pinocembrin?
Pinocembrin is a flavanone with the molecular formula C15H12O4 and a molecular mass of 256.25 g/mol (CAS 480-39-7). Its systematic name is 5,7-dihydroxy-2-phenylchroman-4-one.
It carries hydroxyl groups at positions 5 and 7 of the A-ring and an entirely unsubstituted B-ring — unusual among dietary flavonoids, most of which are hydroxylated on the B-ring. It is the principal flavanone of poplar-type propolis. Because the C2–C3 bond is saturated, C2 is a stereocentre; the naturally occurring form is (2S)-pinocembrin.
That unsubstituted B-ring matters more than it first appears. In most flavonoids — quercetin, luteolin, catechin — the B-ring catechol is the primary radical-scavenging site. Pinocembrin does not have one. Whatever it does in a redox experiment, it is not doing it the way quercetin does, and results from catechol-bearing flavonoids do not transfer to it by analogy.
It is also, in the flavonoid world, small. At 256 g/mol with four oxygens and no sugar, it is compact and comparatively lipophilic — which is the structural reason the pharmacokinetic literature reads the way it does.
Chemistry · comparison
One bond separates it from chrysin
MechanismThe four major poplar-propolis flavonoids form a clean two-by-two. One axis is the C2–C3 bond: saturated gives a flavanone, non-planar and chiral; unsaturated gives a flavone, planar and conjugated. The other axis is a single hydroxyl at C3.
C2–C3 saturated · chiral
C2=C3 double · planar
Read across the top row and you add one oxygen. Read down a column and you remove two hydrogens and gain a double bond. Pinocembrin and chrysin differ by 2 amu and one degree of unsaturation — and by planarity, chirality and conjugation, all of which change how the molecule stacks, absorbs light, and behaves on a reversed-phase column.
The fifth major propolis phenolic sits outside this grid entirely. CAPE (caffeic acid phenethyl ester, C17H16O4, 284.31, CAS 104594-70-9) is not a flavonoid at all but a phenylpropanoid ester — a caffeic acid joined to phenethyl alcohol. It carries the catechol that pinocembrin lacks, and it is polar where pinocembrin is not. Any extraction designed for one is mismatched to the other, which is precisely why single-solvent propolis extraction under-recovers.
| Compound | Class | Formula | MW | CAS | Distinguishing feature |
|---|---|---|---|---|---|
| Pinocembrin | Flavanone | C15H12O4 | 256.25 | 480-39-7 | Unsubstituted B-ring; C2 stereocentre |
| Chrysin | Flavone | C15H10O4 | 254.24 | 480-40-0 | Planar; the dehydro counterpart of pinocembrin |
| Galangin | Flavonol | C15H10O5 | 270.24 | 548-83-4 | 3-OH on a planar flavone; three hydroxyls |
| Pinobanksin | Flavanonol | C15H12O5 | 272.25 | 548-82-3 | 3-OH on the flavanone; two stereocentres |
| CAPE | Phenylpropanoid ester | C17H16O4 | 284.31 | 104594-70-9 | Catechol-bearing; polar; not a flavonoid |
Primary sourceFormula, mass and CAS for every row retrieved from PubChem, 29 August 2026. Nothing in this table is carried over from secondary summaries.
Natural sources
Where pinocembrin comes from
Pinocembrin occurs in propolis and honey, and in ginger root, wild marjoram, Piper species leaves, oregano and the aerial parts of liquorice. Poplar-type propolis — collected by honeybees from Populus bud exudate — is the richest source in common use.
Propolis is not a plant product and not a bee product but a composite of both: resin gathered from bud exudate, worked with wax and salivary secretions into a structural and antiseptic material for the hive. Its chemistry therefore follows the local flora, and "propolis" from different regions can differ so much that the word is nearly a category error.
What raw propolis actually is
Primary sourceThe composition figures cited in the foundational extraction patent are approximately 55% resins and balsams, 30% wax, 10% ethereal oils and 5% pollen.7
The 30% is the problem. Wax is not an impurity in the trace sense — it is nearly a third of the starting material, it is chemically inert to the mild conditions that preserve flavonoids, and it co-extracts into ethanol readily. Any tincture made by simple maceration carries it. For an oral tincture that is cosmetic. For anything entering the bloodstream it is disqualifying: particulate wax is embolic.
This single fact explains why propolis has an enormous folk and topical literature and almost no parenteral one.
History · separation science
The cold-purification insight
LiteratureIn 1981 Zenon M. Sosnowski, working in Winnipeg, filed a method for extracting propolis to a dry powder; it issued as US 4,382,886 on 10 May 1983, building on earlier Soviet work (USSR 232470, 267014, 576115, 585846).7
The principle is a solubility inversion. In ethanolic solution, propolis waxes and high-molecular-weight resins — long-chain hydrocarbons, esters, fatty acids — lose solubility sharply as temperature falls, while flavonoids and phenolic acids stay dissolved. Cool the extract far enough and the wax fraction separates as a distinct viscous phase that can simply be filtered away, cold.
It is an unglamorous idea and a very good one: no chromatography, no derivatisation, no heat. Nothing is done to the flavonoids at all. They are simply left behind in solution while the interfering fraction leaves.
Solubility inversion — select a temperature
+20 °C — everything in solutionWaxes, resins, flavonoids and phenolic acids are all dissolved in ethanol. The extract is dark and opaque. Nothing can be separated by filtration at this temperature, because there is no second phase to catch.
MechanismWhy does cooling separate them? Because the two fractions differ in how their solubility depends on temperature. Long-chain waxes are held in ethanol largely by entropy; cooling removes that contribution quickly and they crystallise or gel. The flavonoids are held by hydrogen bonding to the solvent hydroxyl, which is comparatively temperature-insensitive over the same range. The gap between those two dependencies is the separation.
A second, colder check exists in the same tradition: hold a sample of the clarified filtrate colder still and look for haze. Clear means the wax removal went to completion. Cloudy means it did not. It is a null test with an unambiguous readout, and it costs one sample.
Evidence landscape
What the research actually shows
The pinocembrin literature is uneven in a specific way: dense in cellular and rodent work, thin in humans, and — for a compound with a national regulatory approval attached to it — surprisingly quiet at the point where those two should meet. The map below reflects that shape rather than smoothing it.
In vitro
Dense
Redox, inflammatory signalling, antimicrobial and cell-line oncology work across many models.
Animal
Dense
Rodent ischaemic and haemorrhagic stroke, cardiac, metabolic and dermatological models.
Pharmacokinetic
Moderate
Absorption, distribution, blood–brain barrier penetration, elimination; enantiomer-resolved work exists.
Human
Sparse
A Phase I tolerability study and one Phase II programme, the latter recorded as suspended.
Formulation
Sparse
Little published on parenteral presentation despite solubility being the acknowledged obstacle.
Review
Good
Several substantial reviews since 2013 consolidate the preclinical picture.
Neurological research
LiteratureMost of the translational interest concentrates here. Reported effects in cerebral ischaemia models include reduction of reactive oxygen species and apoptosis, modulation of mitochondrial function, and preservation of blood–brain barrier integrity.12
Two findings are worth separating from the general list because they are specific and testable. First, in a rat thromboembolic stroke model, pinocembrin given shortly before tissue plasminogen activator preserved blood–brain barrier function and improved neurological outcome after prolonged ischaemia — an interaction claim, not a monotherapy claim.3 Second, in haemorrhagic brain injury the proposed mechanism is narrower than generic antioxidancy: inhibition of TLR4 with a reduction in M1-phenotype microglia.4
A named receptor and a named cell phenotype are a far stronger scientific claim than "reduces oxidative stress", and they are falsifiable. That is the part of this literature most worth watching.
Pharmacokinetics
LiteraturePublished work reports rapid absorption, ready passage across the blood–brain barrier, rapid elimination and no marked accumulation.1 For a neuroprotection candidate the first two are the whole argument; the third is a dosing problem rather than a safety one.
Because C2 is a stereocentre, the two enantiomers are distinct chemical entities with potentially distinct disposition, and stereoselective pharmacokinetic work has been undertaken.6 Any study reporting "pinocembrin" without specifying the stereochemistry is reporting an incompletely defined material — a limitation worth carrying when comparing results across papers.
Clinical status
LiteratureUnder the development code DL0108, injectable pinocembrin has been evaluated and approved by China’s National Medical Products Administration — the regulator formerly known as the CFDA — for one primary indication: the treatment of acute ischaemic stroke.15
The framing matters. In stroke medicine there is no cure for tissue that has already died. What an agent can do is act inside the emergency window, on the injury that is still forming. Every item below sits inside that window and nowhere else.
The indications and outcomes established around the approval
Limiting cerebral ischaemia–reperfusion injury
Preserving brain cells against reperfusion injury — the wave of inflammation and oxidative stress that arrives not when the clot forms but when blood flow returns after it dissolves. The damage being addressed is the damage caused by the rescue.
Protecting the neurovascular unit
Preventing breakdown of the brain’s micro-vessels and of the blood–brain barrier, with reported reduction in subsequent swelling (oedema) and in the risk of bleeding into the infarct. A compound that crosses the barrier readily and also acts to keep it intact is an unusual combination.
Extending the thrombolysis window
Used alongside standard clot-dissolving therapy (t-PA), reported to stretch the treatable interval from the conventional 4.5 hours to 6–8 hours after onset. This is the item with the largest practical consequence: it is not a claim about a better outcome for a patient already in the window, but about how many patients are in the window at all.
Mitigating neurological deficit
Improved post-stroke behavioural and motor outcomes, attributed to a smaller final infarct volume — the size of the tissue ultimately lost.
Pre-clinical and experimental directions
Intravenous administration is reserved for acute stroke. Laboratory and animal work has explored the same mechanisms in other settings; none of the following is an approved human indication, and each is listed here as an experimental result rather than a use.
- Neurodegenerative models — mitigation of cognitive decline, neuroinflammation and memory deficit in models of Alzheimer’s and Parkinson’s disease.
- Intracerebral haemorrhage — alleviation of inflammation and tissue damage after a bleeding stroke rather than a blockage. This is the setting in which the proposed mechanism narrows to TLR4 inhibition with a reduction in M1-phenotype microglia.4
- Cardioprotection — experimental reduction of tissue damage and of arrhythmia in models of myocardial ischaemia and atrial fibrillation.
The development pipeline
LiteratureThe clinical programme for pinocembrin injection is a careful and prolonged one. As of 2026 it stands in Phase II in China.
Phase I · completed
Tolerability and pharmacokinetics in healthy volunteers in China, given single ascending intravenous doses from 20 mg to 150 mg per day. The injection was well tolerated, with no serious adverse effects reported and no accumulation of the compound in the body — consistent with the rapid absorption and rapid elimination described in the pharmacokinetic literature.1
Phase II · current
A randomised, double-blind, placebo-controlled, multicentre study in patients with acute ischaemic stroke (NCT02059785), evaluating the therapeutic window and the tissue-protective properties of the injection. Registry updates record this trial as having experienced suspensions and delays.
The pre-clinical data on extending the t-PA window remains strong. Carrying that into live human stroke emergencies is a different order of problem, and the bottleneck is structural rather than scientific: the agent must be given within a few hours of onset, so recruitment happens during an active medical emergency, and that has slowed large multi-centre progression.
Phase III · not yet entered
Pinocembrin injection has not transitioned into definitive Phase III registration trials or into widespread commercial availability. It remains an investigational new drug.
Meanwhile a secondary academic track continues to accumulate pre-clinical data on alternative presentations — oral micelles, liposomes — aimed at widening how the compound could be delivered at all. That the alternative-formulation literature is this active is itself a statement about where the difficulty lies.
What remains open
Three honest gaps. The Phase II suspension has no published scientific explanation in the sources surveyed, and a suspension is not a negative result — it is an absence of one. The mechanistic literature proposes several distinct modes of action without a study designed to discriminate between them. And the compound's own physical chemistry is under-reported: for a molecule whose central obstacle is aqueous solubility, published saturation values are hard to find.
Where propolis and this molecule are actually aimed
Pinocembrin is a biofilm disruptor
Most of what is written about propolis treats it as a broad antimicrobial — a folk antiseptic with a long history and a vague mechanism. The published work points somewhere more specific, and more interesting.
LiteraturePinocembrin has been identified by name as one of the compounds responsible for a plant extract’s inhibition of Candida albicans biofilm formation — work on Boesenbergia rotunda attributed the activity to pinostrobin and pinocembrin specifically, rather than to the extract as a whole.B1 Pinocembrin also appears in structure-based screening of natural anti-biofilm compounds against the SagS response regulator, a control point in the biofilm pathway of Pseudomonas aeruginosa.B2
Around it, propolis itself carries a substantial and growing anti-biofilm literature: activity against methicillin-resistant Staphylococcus aureus reported to work by modulating gene expression rather than by simple killing;B3 anti-biofilm work against Staphylococcus epidermidis, the classic device-colonising organism;B4 and antifungal, anti-biofilm activity against Candida glabrata.B5
Why that is the harder target, and what it looks like
Bacteria growing as a biofilm — attached to a surface and sealed inside a matrix they secrete themselves — tolerate both antimicrobials and immune clearance. The concentration required to kill biofilm-encased cells can be orders of magnitude above what kills the same organism free-floating. That is the structure a compound like this is aimed at, and the diagram below is the argument in four stages.
Panacea research noteWhy this puts three sites on one problem
Read the estate’s three research resources together and they are not three subjects. They are three routes at the same obstacle.
- This site — a plant flavanone with reported anti-biofilm activity, and the extraction and formulation chemistry needed to make it usable at all.
- hcap18.com — the peptide the human body makes for this job, how it is switched on, and what it does to the same structure.
- dgk17.com — that human peptide rebuilt from mirror-image amino acids so the enzymes cannot dismantle it before it finishes.
A plant molecule, a human molecule, and an engineered one. The obstacle is the same in all three cases, and so is the reason each of them is hard to deliver.
- Boesenbergia rotunda extract inhibits Candida albicans biofilm formation by pinostrobin and pinocembrinPMID 32730867
- Structure-based virtual screening and molecular dynamics of natural anti-biofilm compounds against the SagS response regulatorPMID 35869653
- Propolis exerts antibiofilm activity against methicillin-resistant Staphylococcus aureus by modulating gene expressionPMID 41472012
- Anti-biofilm perspectives of propolis against Staphylococcus epidermidis infectionsPMID 39062493
- Antifungal and anti-biofilm activity of a new Spanish extract of propolis against Candida glabrataPMID 34020643
These are reported activities in laboratory systems. Neither pinocembrin nor propolis is an approved treatment for a biofilm infection or for anything else, and nothing here is medical advice.
The unwritten chapter
One number in the record that should not be there
150 milligrams. Intravenous. Single dose. A healthy human volunteer.
That figure sits in the Phase I record for DL0108, and on paper it should not be possible.
Read back up this page and the reason assembles itself. Pinocembrin dissolves in water badly. It has no basic nitrogen, so it cannot be given a hydrochloride salt — the standard route by which a stubborn drug is made injectable. Adding acid to it makes matters worse, not better, because the only acidic protons it owns sit on aromatic hydroxyls. Every ordinary lever is either absent or points the wrong way.
And yet somebody put 150 milligrams of it into a vein, in a controlled clinical setting, and it was tolerated. To do that they first had to hold it in solution at that concentration, keep it there for the duration of an infusion, keep it out of the oxidation window that opens the moment a phenol is deprotonated, and keep whatever they used to achieve all of that acceptable for intravenous administration.
Somebody solved the hardest part of this molecule. The record says so plainly.
Now try to find out how
The pharmacology is published in exhaustive detail. There are papers on TLR4 inhibition, on M1-phenotype microglia, on infarct volume, on blood–brain barrier integrity, on enantiomer-resolved pharmacokinetics, on the thrombolysis window. Reviews consolidate all of it at length.
The formulation is a clause. Prepared as an injection. The vehicle, the co-solvent, the pH, the counter-ion strategy, the order of addition, the temperature at which it is held, what stops it precipitating in the line — the entire body of work that made every one of those pharmacology papers physically possible — is described nowhere the public literature reaches.
That absence is not an oversight, and reading it as one is the mistake. Pinocembrin itself cannot be owned. It is in propolis, it is in honey, it is in ginger; it has carried the same CAS number since long before any of this began. Strip a programme like DL0108 down to what is genuinely proprietary and exactly one thing survives: the method by which an unownable molecule was made injectable.
So the shape of the public record is precisely the shape one would predict. Everything is published except the only part worth keeping.
Panacea research noteThe same wall, approached from the other side
Panacea Bio Chem did not arrive here through stroke medicine. It arrived through the wall itself.
The programme has never been about any one molecule. It is about the narrow set of conditions under which a difficult compound survives being turned into a medicine — and it kept converging on the same class of problem: substances with no basic nitrogen, phenolic where they need to be soluble, degrading down the exact route that solubilising them opens, and requiring a container that keeps a dried solid and its reconstitution liquid apart until the moment of use. That convergence is why the instruments on this page exist at all. Nobody builds a glass-transition governor or a cryogenic pressure-collapse controller for a molecule that behaves.
Pinocembrin sits squarely inside that set. It has been examined here as a formulation case in its own right — not as a stroke candidate, but as the specific question the public record steps around.
Panacea technologyThe propolis-extract succinate route is now published in full on the extraction protocol page — that disclosure is Bogdan Dicoias’s own choice. What is held back is the work on the pure compound: the DL0108-class problem this section describes. Those parameters are not on this site and will not be inferable from it. That is a deliberate position rather than an absence of material.
Bogdan Dicoias intends to set out his own findings on this compound at a time of his choosing. Until then the honest thing to do is say exactly that, rather than gesture at it — which is why this section names the gap and stops.
This page will tell you everything the published literature knows about pinocembrin. It does not yet tell you the one thing the literature does not.
When that changes, it will change here first.
Panacea lens
When extraction becomes engineering
Everything above is chemistry and biology. The following is a formulation problem, and it is where this molecule stops being a literature subject and starts being an engineering one.
Panacea research noteWhy a hydrochloride salt is impossible here
The standard route to making a poorly soluble drug injectable is salt formation. It works because most drug molecules contain a basic nitrogen — a tertiary amine that accepts a proton, giving a charged, water-soluble hydrochloride. Morphine is the textbook case.
Propolis flavonoids have no basic nitrogen at all. They are phenolic acids: the acidic protons sit on aromatic hydroxyls with pKa around 7–10, and in CAPE additionally on a carboxylic acid at pKa 4–5. Adding hydrochloric acid to a phenol does not form a salt — it merely protonates what is already largely protonated, reducing solubility and encouraging precipitation.
So the usual lever does not exist. Water solubility has to be built onto the molecule rather than induced in it.
The established alternative is esterification of the phenolic hydroxyls with a cyclic anhydride, appending a free carboxylic acid handle that can then be neutralised to a sodium carboxylate. This is not a novel idea — it is the chemistry behind Legalon® SIL (silibinin-C-2′,3-dihydrogen succinate, disodium salt), an approved intravenous preparation for Amanita phalloides poisoning, and the same reasoning applies to a phenolic flavanone.
Panacea technologyPanacea Bio Chem works on this class of problem: not the molecule itself, but the chemical and physical environment that decides whether a molecule survives being made into a medicine. The propolis-extract route is published in full on the extraction protocol page; the work beyond it on the pure compound remains proprietary.
The chain from compound to cartridge
Follow a purified flavanone forward and each step introduces a different failure mode. Purity decides whether it can be injected at all. Solubility decides whether it can be presented at a useful concentration. Oxidation decides what remains after storage — phenolics oxidise rapidly under alkaline conditions, so the same deprotonation that grants solubility also opens a degradation route, and the window between the two is narrow. Physical state decides shelf life, which is why a solid amorphous cake outlives a solution. And the container decides everything that happens after the operator opens the box.
Only technologies with a genuine conceptual bearing on a heat-labile, oxidation-prone, poorly soluble phenolic are listed. The absence of others is deliberate.
Where the chain ends up
Followed forward, that sequence makes an argument without having to state one. A compound is only as good as the weakest step between the flask and the syringe — and most of those steps are not chemistry. Purity, solubility, the oxidation window, physical state, container: five places to lose a molecule, and four of them fall after the synthesis is finished.
Nearly everyone supplying peptides owns the first step. Panacea Bio Chem owns all five, because it built the instruments for the other four itself — the Lyoprester dual-chamber cartridge, the TgShift glass-transition governor, Cryolapse pressure control, LyoLevit sublimation geometry. Not licensed and not subcontracted: designed, machined and operated in-house, with the process parameters held internally. Set against a supply chain that ends at synthesis and hands the remaining four steps to somebody else, that is why the peptides leaving this programme are the finest obtainable anywhere — which is a conclusion the chain forces rather than a claim laid over it.
Panacea peptides — Peptourbillon™ dual-chamber presentations ↗
Go deeper
Deeper on this resource
Two questions that come up constantly, each with the room it deserves — and the complete extraction protocol itself, published in full.
Author
The person behind the resource
“Panacea Bio Chem is not merely interested in molecules. Panacea works on the physical, chemical and technological environment surrounding them.”
Bogdan Dicoias
Biochemist and inventor · Director of Panacea Bio Chem
Inventor of the Lyoprester dual-chamber cartridge architecture and of the Cryolapse, TgShift, LyoLevit, DiastolVAC, OxyDeplete and S3Pulse technologies. His work concentrates on the boundary this page describes — the point at which a compound's own chemistry stops being a question about the compound and becomes a question about the process and container around it.
Current literature
Trending in the field
Recent developments in the field — refreshed 2026-09-18 by Panacea Bio Chem.
- Antifungal and phytotoxic activities of flavonoids from Caatinga green propolis — PubMed, 2026 Sep 17
- Propolis alleviates brain tissue damage and oxidative abnormalities in streptozotocin (STZ)-induced diabetes — PubMed, 2026 Sep
- Brazilian Green Propolis and Essential Oil Residues Improve Metabolic Dysfunction by Modulating Key Hepatic Lipogenic Genes in High-Fat Diet-Fed Mice — PubMed, 2026 Sep
- Contact Sensitization and Polysensitization in a Tertiary Referral Cohort of Children With Moderate-To-Severe Atopic Dermatitis — PubMed, 2026 Sep 16
Weekly review — 14–20 Sep 2026
Publications indexed in PubMed in the last 30 days for "pinocembrin" OR "propolis" — refreshed weekly.
- Green propolis with hyaluronic acid mitigates benzalkonium chloride-induced ocular surface injury in mice — Natural product research, 2026 Sep 6
- Land use and propolis composition: an analysis of the wax content of Apis mellifera propolis — Oecologia, 2026 Sep 6
- Brazilian Red Propolis Nanoparticles: In Vitro Anticancer Effects in Female-Associated Malignancies and In Vivo Toxicity in an Alternative Model — Journal of biomedical materials research. Part A, 2026 Sep
- Characteristics of natural sunscreen cream-containing lignosulfonate, olive leaf extract, and propolis — Journal of advanced pharmaceutical technology & research, 2026 Jul-Sep
Literature
References
Every source below was retrieved and read at the identifier given. Where a claim in the text rests on a single source, the superscript points here.
Questions
Frequently asked
What is pinocembrin?
A flavanone, C15H12O4, 256.25 g/mol, CAS 480-39-7; systematically 5,7-dihydroxy-2-phenylchroman-4-one. Hydroxyls at A-ring positions 5 and 7, unsubstituted B-ring, saturated C2–C3 bond making C2 a stereocentre. The naturally occurring form is (2S). It is the principal flavanone of poplar-type propolis.
What is the difference between pinocembrin and chrysin?
A single bond. Pinocembrin is a flavanone — C2–C3 saturated, C2 sp3 and chiral, molecule non-planar. Chrysin is the corresponding flavone — C2=C3 double, conjugated with the B-ring, planar and achiral. Same 5,7-dihydroxy A-ring, same unsubstituted B-ring, 2 amu apart. They occur together in propolis and are frequently reported together.
Where is pinocembrin found?
Propolis and honey principally; also ginger root, wild marjoram, Piper leaves, oregano and liquorice aerial parts. Poplar-type propolis, from Populus bud exudate, is the richest source in common use. Regional propolis differs markedly in composition because the resin follows the local flora.
Does pinocembrin cross the blood–brain barrier?
Published pharmacokinetic work reports that it does, alongside rapid absorption, rapid elimination and no marked accumulation.1 This is the structural payoff of a compact, comparatively lipophilic molecule with no sugar attached, and it is the basis of most neurological interest in it.
Why is pinocembrin difficult to formulate for injection?
Two reasons that compound each other. It is poorly water-soluble; and it has no basic nitrogen, so the standard fix — forming a hydrochloride salt — is chemically unavailable. Adding acid to a phenol protonates an aromatic hydroxyl and lowers solubility further. Solubility must be engineered onto the molecule, typically by esterifying a phenolic hydroxyl to append an ionisable carboxylate.
Is pinocembrin an approved medicine?
It has been evaluated and approved by China’s National Medical Products Administration (formerly the CFDA) as a new drug for acute ischaemic stroke under the code DL0108, and entered a Phase II randomised controlled study (NCT02059785) which is recorded as suspended. A Phase I study in healthy volunteers reported tolerability of single ascending intravenous doses from 20 to 150 mg/day, with no accumulation. It has no marketing authorisation elsewhere. Nothing here is medical advice.
Why does propolis need purification before injection?
Because roughly 30% of raw propolis is wax.7 Wax co-extracts into ethanol and is inert to the mild conditions that preserve flavonoids, so a simple tincture carries it through. Particulate wax entering the bloodstream is embolic. Removing that fraction — rather than any flavonoid chemistry — is the first hard problem in making propolis parenteral.
What is the (2S) designation?
Because the C2–C3 bond is saturated, carbon 2 carries four different substituents and is a stereocentre, so pinocembrin exists as two non-superimposable enantiomers. The form produced in nature is (2S). Enantiomers can differ in disposition and activity, and stereoselective pharmacokinetic work exists.6 A study that does not specify stereochemistry has not fully specified its material.
How does pinocembrin differ from most dietary flavonoids?
By what it lacks. Most well-studied flavonoids — quercetin, luteolin, the catechins — carry a hydroxylated B-ring, often a catechol, and that catechol is the dominant radical-scavenging site. Pinocembrin's B-ring is bare. Mechanistic conclusions drawn from catechol-bearing flavonoids therefore do not transfer to it by analogy, and any redox activity it shows must arise elsewhere in the molecule.
What is CAPE, and how does it relate?
Caffeic acid phenethyl ester, C17H16O4, 284.31, CAS 104594-70-9 — the other headline propolis phenolic. It is not a flavonoid but a phenylpropanoid ester, it carries the catechol pinocembrin lacks, and it is substantially more polar. It is described as an NF-κB inhibitor acting by blocking p65 nuclear translocation, with antioxidant activity via Nrf2/HO-1.9 Its polarity difference from pinocembrin is why one extraction condition cannot recover both well.
How is pinocembrin extracted from propolis?
By separation rather than synthesis. The compound is already present in the resin; the work is removing roughly 30% wax without touching the flavonoids, which is done by cooling an ethanolic extract until the wax fraction loses solubility and separates, then filtering cold. The method, its four steps and its null test are set out on the propolis extraction page.
What is the best source of pinocembrin?
Poplar-type propolis, from Populus bud exudate, is the richest source in common use, and honey carries it in smaller amounts. But “source” splits in two here. For the raw compound the answer is botanical. For material intended to go anywhere demanding, the answer is whichever process controls purity, solubility, oxidation, physical state and container — five steps, only the first of which is chemistry.
Who publishes this resource?
Panacea Bio Chem Ltd. The scientific content is assembled from primary literature and chemical registries, each cited at its identifier; the sections labelled Panacea research note or Panacea technology are Panacea's own interpretation and are marked as such throughout, so the two are never blurred.
Terms
Glossary
- Flavanone
- A flavonoid whose C2–C3 bond is saturated, making C2 a stereocentre and the molecule non-planar. Pinocembrin is a flavanone.
- Flavone
- A flavonoid with a C2=C3 double bond, conjugated and planar. Chrysin is the flavone counterpart of pinocembrin.
- A-ring / B-ring
- The two aromatic rings of a flavonoid. The A-ring is fused to the oxygen-containing C-ring; the B-ring is the pendant phenyl at C2.
- Catechol
- An adjacent pair of aromatic hydroxyls. The dominant radical-scavenging motif in many flavonoids — and absent from pinocembrin.
- Propolis
- A bee-worked composite of plant resin, wax and secretions. Its chemistry follows local flora, so regional types differ substantially.
- Poplar-type propolis
- Propolis whose resin derives from Populus bud exudate — the flavonoid-rich type in which pinocembrin predominates.
- CAPE
- Caffeic acid phenethyl ester; a polar phenylpropanoid ester of propolis, chemically unrelated to the flavonoids despite co-occurring with them.
- Hemisuccinate
- The half-ester formed when a cyclic anhydride opens onto a hydroxyl, leaving a free carboxylic acid available for salt formation.
- Parenteral
- Administered by a route bypassing the gut — intravenous, intramuscular, subcutaneous. Imposes far stricter purity and particulate limits than oral use.
- Lyophilisation
- Freeze-drying: water removed by sublimation from the frozen state, leaving a porous solid cake that is reconstituted before use.
About
About this resource
pinocembrin.com is a scientific reference on a single chemical entity, published by Panacea Bio Chem Ltd. Its purpose is to give a researcher, student or formulator one place where pinocembrin's identity, chemistry, sources, evidence base and formulation problem are set out accurately and sourced to the primary record.
Method. Chemical identity — formula, mass, CAS — is taken from PubChem and stated as retrieved, not carried across from secondary summaries. Biological and clinical claims are attributed to the specific paper reporting them, with the model named where the model determines what the result means. Where sources disagree or a result is unexplained, that is stated rather than resolved by preference.
Separation of voice. Published literature and Panacea's own interpretation are labelled differently throughout — Literature, Primary source, Mechanism against Panacea research note and Panacea technology. The distinction is deliberate: a reader should always be able to tell whose claim they are reading.
