Gut Health & Nutrition Library · Technical Article

Potassium Diformate in Swine and Poultry Diets: Dose–Response Evidence, Tolerance and Regulatory Status

By the SKF Bio technical team · Reviewed against 33 primary studies and EU regulatory texts · Last updated: 28 September 2026 · Reading time: ~14 min · Evidence level: peer-reviewed primary trials + one industry data set (flagged)

1. What is potassium diformate?

Potassium diformate (KDF), CAS 20642-05-1, is a hydrogen-bonded 1:1 double salt of formic acid and potassium formate with the formula HCOOH·HCOOK and a relative molecular mass of 130.14. It is a white crystalline powder that is freely soluble in water, stable under acidic conditions and dissociates into formic acid and potassium formate at neutral to slightly alkaline pH. Commercial feed-grade material typically assays at 95–98%.

The compound is not a mixture and not a simple salt: the formic acid and potassium formate molecules are joined by an intermolecular hydrogen bond, giving what Chinese process literature describes as a "double-acid" or dimer structure. ^[7],[8] This single structural detail explains most of its feeding behaviour, because a hydrogen-bonded dimer behaves very differently in the gut from a free acid applied at the same inclusion rate.

Table 1. Identity and physical properties of potassium diformate

Note that formic acid's pKa of 3.75 sits below that of benzoic acid (4.21), acetic acid (4.76), propionic acid (4.88), lactic acid (3.86) and sorbic acid (4.76), which is why formate-based systems acidify more per kilogram than most alternatives. Published minimum inhibitory concentrations for KDF cluster in the range 1.95–6.25 mg/mL depending on strain panel and method; in one screen of 15 clinical isolates the breakpoint coincided exactly with the point at which medium pH began to fall, linking the antimicrobial effect to acidification rather than to a specific receptor. ^[7],[22]

2. How does potassium diformate work?

KDF acts through four linked routes: it survives the stomach largely intact and releases formic acid in the intestine; undissociated formic acid crosses bacterial cell walls and collapses the pathogen proton gradient; lower pH improves protein digestion and nutrient absorption; and the released potassium supplies electrolyte. Its effect on gut pH is real but both site- and species-dependent, and several well-run trials report no pH change at all.

2.1 The molecule survives the stomach, then releases in the intestine

Because the hydrogen-bonded dimer is stable in acid, most of the ingested dose passes the stomach without dissociating. Chinese reviews consistently place the figure at "85% or more" of the dose reaching the duodenum intact, where the near-neutral pH allows it to release formic acid, formate and K⁺. ^[7] This is the property formulators actually pay for: it shifts acid delivery from the stomach (where excess acid suppresses feed intake and damages mucosa) into the small intestine and hindgut, where pathogenic load matters most.

A head-to-head broiler trial makes the practical consequence explicit. Comparing formic acid and KDF at 5 g/kg for 35 days, KDF produced the greater response precisely because "KDF permits a proportion of FA to pass through the fore-gut intact and enter the small intestinal tract", whereas most ingested formic acid is absorbed or metabolised before it gets there. ^[4]

2.2 Acidification is real but segment-dependent — report it honestly

The acidosis narrative is often overstated. Measured results depend heavily on sampling site and species:

Table 2. Reported effects of potassium diformate on digestive-tract pH

The negative results are the useful ones commercially. In the weaned-piglet study above, performance-independent endpoints still moved — digesta formic acid concentration rose sharply and bacterial counts fell — so the mode of action clearly does not require a measurable drop in bulk pH. ^[2] Likewise, KDF-supplemented broilers showed large and significant increases in intestinal lipase, amylase and trypsin activity while the pH of the digesta they produced was unchanged. ^[10] A defensible claim, therefore, is "increases intestinal formate availability and digestive enzyme activity", not "lowers gut pH".

2.3 Antibacterial action: two components, one target

The antimicrobial effect combines (i) undissociated formic acid penetrating the bacterial cell wall and releasing protons into the cytoplasm, forcing ATP-consuming proton extrusion, depleting cellular energy and blocking nutrient transport, and (ii) the formate anion acting on cell-wall protein. ^[7],[22]

In vivo confirmation is consistent. In growing-finishing pigs fed 12,000 mg/kg, coliform counts fell in the duodenum (P < 0.03), jejunum (P < 0.02) and rectum (P < 0.10). ^[1] In piglets fed 18,000 mg/kg, KDF lowered total anaerobic bacteria, lactic acid bacteria, coliforms and yeasts in stomach, distal small intestine, caecum and colon contents (P ≤ 0.04). ^[2] A murine infection model provides the sharpest evidence: mice receiving 10 g/kg KDF in feed for two weeks, then challenged with Salmonella Typhimurium ATCC14028 at 1.25 × 10⁸ CFU, showed significantly reduced bacterial load in blood and caecal tissue (P < 0.05) together with lower serum IL-6, IL-12 and TNF-α (P < 0.05). Notably, 0.1% KDF in drinking water outperformed 1% in feed — a 10-fold lower dose because the water route bypasses feed-matrix buffering. ^[22]

2.4 Barrier, immunity and the Keap1–Nrf2 and NF-κB axes

Beyond acidification, KDF modulates documented signalling cascades. In broilers, 1,000 mg/kg raised hepatic catalase activity (29.8 → 32.0 U/mg protein at 21 d, P < 0.05) and simultaneously up-regulated NRF2 and down-regulated KEAP1 gene expression (both P < 0.05) — a coherent Keap1–Nrf2 antioxidant activation rather than an isolated enzyme reading. ^[14]

In grass carp challenged with Aeromonas hydrophila, KDF improved every measured barrier and immune endpoint: intestinal lysozyme rose from 61.6 to 118.3 U/mg protein and complement C3 from 36.6 to 83.0 mg/g protein, while myeloperoxidase fell from 0.95 to 0.64 U/g wet tissue (all P < 0.05); enteritis incidence fell significantly. Mechanistically the same animals showed down-regulation of TLR4, MyD88, IRAK4, TAK1, TRAF6, IKKβ/γ and NF-κB p65 with up-regulation of IκBα, alongside down-regulation of the RhoA/ROCK/MLCK/p38 MAPK axis that governs tight-junction opening. ^[20],[21] Dataset: 1,620 fish, six dose levels, 70 days.

2.5 Potassium supply

KDF delivers roughly 27–30% elemental potassium by mass. Beyond its role in intracellular osmolarity and the activation of more than 60 enzymes, potassium adequacy matters in modern low-crude-protein diets: soybean meal is the dominant potassium source in pig and poultry rations, so high-crystalline-amino-acid formulations that reduce soybean inclusion can become marginally deficient in potassium. ^[7],[30]

3. What does the evidence show in pigs?

In weaned piglets the strongest single result is on diarrhoea: graded doses cut the faecal score index by 77% over 10 days at 8,000 mg/kg (n = 120, P < 0.05). Growth responses are real but dose-thresholded — 4,000 mg/kg was ineffective in the same trial while 8,000 mg/kg moved both ADG and feed intake. In grow-finishers, historical European work shows carcass leanness gains, but recent North American work on the closely related sodium salt failed to reproduce it, so results should be presented as conditionally positive.

3.1 Weaned piglets: growth, diarrhoea and immunity

A 2023 Chinese trial run under commercial conditions provides the cleanest recent dataset. One hundred and twenty Duroc × Landrace × Large White piglets weaned at 8.16 ± 0.40 kg were assigned to three treatments (4 pens × 10 pigs per pen) and fed 0, 4,000 or 8,000 mg/kg KDF for 10 days. ^[9]

Table 3. Dose–response of potassium diformate in weaned piglets (n = 120; 10 days; initial BW 8.16 kg) — data from Zeng et al., 2023 ^[9]

Two features matter commercially. First, there is a clear threshold between 4,000 and 8,000 mg/kg — the lower dose was statistically indistinguishable from control on every endpoint, so a "cheaper low dose" formulation should not be assumed adequate. Second, the authors themselves flagged that feed conversion did not improve, against published precedent; the plausible reason they give is the very short 10-day window. ^[9] Reporting both facts strengthens rather than weakens the case.

The accompanying protein-sparing pattern is mechanistically coherent: total protein up while urea nitrogen falls is the signature of reduced amino-acid catabolism and increased deposition, and it matches the +7.1% ADG rather than floating free of it.

3.2 Growing-finishing pigs and carcass

The foundational European dataset remains Øverland et al. (2000). Across three experiments, 0.8% K-diformate increased overall ADG versus control; in a 96-pig dose titration (0, 6,000, 12,000 mg/kg) both ADG and ADFI rose linearly (P < 0.01), carcass fat percentage fell (linear P < 0.03) and lean percentage rose in ham (P < 0.01), flank (P < 0.02), loin and neck/shoulder (P < 0.09). Stomach lesion scores were unaffected. ^[1]

In a comparator trial against benzoic acid, piglets receiving 12,000 mg/kg KDF performed equivalently to those on benzoic acid at 10 g/kg, which itself exceeded control by 9% feed intake, 15% weight gain and 6% better FCR. ^[3]

3.3 Sows and gestating animals

The EU's current zootechnical authorisation covers sows at up to 12,000 mg/kg complete feed, which is itself an endorsement of a recognised performance effect in that category. ^[27] Published summary data indicate that KDF inclusion at this level is associated with reduced sow body-weight loss and improved litter weaning weight. ^[7] Specific independent trial detail in this category is thin, and we do not treat it as an established quantitative endpoint.

4. What does the evidence show in broilers?

Broiler data are the most robust in the KDF literature. Two Chinese Academy of Agricultural Sciences trials published in 2024 used 180 and 360 birds respectively: 2,000 mg/kg improved full-cycle F/G from 1.57 to 1.51 (P < 0.001) plus crude-protein metabolic rate from 51.5% to 56.8% (P < 0.001), while 40,000 mg/kg — roughly ten times commercial use — caused growth depression but no organ toxicity. Independent work in 800 birds found 6,000 mg/kg optimal, improving ADG 6.7% and dressing percentage by 1.7 percentage points.

4.1 Growth performance and nutrient utilisation

Table 4. Key potassium diformate broiler trials — design and outcomes

The inverted-U shape across doses is the single most practical takeaway. Four independent trials converge on an optimum between roughly 2,000 and 6,000 mg/kg, with diminishing or reversed returns above that. The 2021 trial using 800 birds is particularly informative because its top dose (9,000 mg/kg) was clearly worse than 6,000 mg/kg on every aggregate endpoint — the highest available KDF dose is not the best.

4.2 Nutrient digestibility — the mechanism behind the F/G gain

Apparent metabolic-rate data measured by TiO₂ marker and total faecal collection (days 39–42) in the Chen X. trial are worth reproducing in full because they convert performance claims into a mechanistic story ^[10]:

Table 5. Nutrient apparent metabolic rate in broilers at 42 days (%)

The same trial measured digestive enzymes and found dose-dependent increases throughout — duodenal amylase 2.45 → 3.18 U/g, ileal lipase 3.78 → 5.55 U/g, jejunal trypsin 1.78 → 2.34 U/g (all P < 0.001) — while, as noted, digesta pH did not change. Intestinal morphology improved in parallel: jejunal villus height rose from 976 to 1,152 µm and villus:crypt ratio from 4.47 to 5.29 (both P < 0.001). ^[10]

4.3 Microbiome composition at 16S resolution

The highest-resolution poultry data come from full-length 16S rDNA sequencing of caecal contents. At 3,000 mg/kg, KDF reshaped community structure substantially ^[15]:

Table 6. Caecal microbial composition in broilers fed 3,000 mg/kg potassium diformate (relative abundance, %)

A falling Firmicutes : Bacteroidetes ratio and reduced Proteobacteria are both directionally favourable, though this is compositional rather than functional evidence and no causal link to the performance response was established.

4.4 Target-animal tolerance: the safety ceiling is high

This is the strongest safety asset in the file. Following China's official Guidelines for Tolerance Tests in Target Animals, 360 mixed-sex Arbor Acres birds (3 × 6 replicates × 20) received 0, 4,000 or 40,000 mg/kg KDF for 42 days — the high dose being ten times the 4,000 mg/kg reference and five times the top of the typical 1,000–8,000 mg/kg commercial window. ^[11]

Table 7. Tolerance study: 4,000 vs 40,000 mg/kg potassium diformate in broilers (n = 360; 42 days)

Despite a 25% drop in growth at the overdose level, no target-organ toxicity, no organ-index change and no tissue lesion appeared. The authors' conclusion — that broiler tolerance to KDF lies "below 40 g/kg" with 4 g/kg showing no adverse effect — is conservative and should be quoted as such. ^[11] Some haematological shifts did reach significance at the overdose level (platelet count and plateletcrit reduced at 42 d, P = 0.023–0.033; urea up, uric acid down at 21 d), consistent with a metabolic-cost-of-detoxification picture rather than organ damage. ^[11]

Independently, EFSA's FEEDAP Panel reviewed the tolerance data set for its 2022 renewals and specifically reduced its maximum safe level for weaned piglets to 6,000 mg/kg complete feed, extending the same conclusion to pigs for fattening — while maintaining 12,000 mg/kg for sows. ^[28]

5. Laying hens, rabbits and fish: how far does the effect transfer?

Yes, but the optimal dose drops and the endpoint changes. In late-lay hens, 10,000 mg/kg increased hen-day egg production by 27% and cut mortality 73% (n = 400, P = 0.0245 and 0.0317) with parallel falls in circulating and hepatic lipid. In grass carp the optimum is 3,000–4,500 mg/kg. In rabbits, benefits appeared only when KDF was combined with benzoic acid. Effects are real across species, but not transferable without re-establishing the dose.

5.1 Late-laying hens: production, lipid metabolism and mortality

Four hundred Hy-Line Brown hens at 65 weeks of age were fed 0, 5,000, 10,000 or 20,000 mg/kg KDF (≥98% purity) for eight weeks. ^[18]

Table 8. Potassium diformate in late-phase laying hens (n = 400; 8 weeks) — Li & Pan, 2025 ^[18]

The gene-expression pattern is mechanistically tidy: lipogenesis genes FASN and ACC down-regulated while CPT-1 (fatty-acid β-oxidation) rises, matching the fall in hepatic lipid. This is the relevant mechanism for fatty-liver-related drops in late lay. Note that the authors identify 10,000 mg/kg — not the top dose — as optimal; 20,000 mg/kg was numerically worse on production.

A separate master's-level trial in 648 hens fed 1,000 or 2,000 mg/kg reported significant increases in feed intake (132.1 → 143.4 g/d, P = 0.0096) and eggshell proportion (10.32% → 10.69%, P = 0.0422), numerically higher egg production, reduced duodenal IL-22 and TNF-α expression (P < 0.05) and higher serum IgM (P = 0.0054), but concluded there was no dose dependence and no synergistic effect when combined with a soil-derived Bacillus. ^[19] Both studies agree on direction but differ in magnitude; do not average them.

5.2 Aquaculture: grass carp as the best-characterised fish model

Two large Sichuan Agricultural University theses share one growth experiment (1,620 juvenile grass carp, six doses, 70 days) but report different endpoints, so they should be cited as one dataset with two layers rather than as independent replicates. ^[20],[21] Starting weight was 5.73 g.

Table 9. Dose titration of potassium diformate in juvenile grass carp (n = 1,620; 70 days; initial BW 5.73 g)

Quadratic regression across endpoints places the optimum at 3,600–4,100 mg/kg, with the enteritis-incidence model giving 3,830 mg/kg (R² = 0.805). ^[20],[21] Above approximately 6,000 mg/kg the benefit erodes: at 7,500 mg/kg several barrier proteins returned to control levels and histological examination showed renewed inflammatory infiltration in the spleen. ^[21] Interestingly, surviving 7,500 mg/kg animals still grew, because FCR was unaffected by dose — the cost of over-supplementation shows up in health markers before it shows up in growth.

A 2024 open-access review pooling aquatic species finds the same practical band: 2,000–3,000 mg/kg in European sea bass, 1,000–3,000 mg/kg in Nile tilapia, 1,000–2,000 mg/kg in sturgeon. ^[5]

5.3 Rabbits — and the limits of attribution

In 200 weaned Rex rabbits (single-cage housed, 56 days), diets supplying 10,000 mg/kg KDF plus 2,000 mg/kg benzoic acid increased ADG from 19 to 21 g (P = 0.009) and improved feed : gain from 5.33 to 4.84 (P = 0.008); crude-protein digestibility rose 6.9% (P = 0.048), ether extract 5.0% (P = 0.006) and NDF digestibility 17.2% (P = 0.008). Stomach and caecal pH were not significantly affected. ^[23]

5.4 Drinking-water application

A 54-day trial in 480 native hybrid (local crossbred) male chickens tested KDF in drinking water at 350, 550 and 750 mg/L. Growth performance and immune organ indices were unaffected at every level (all P > 0.05), but intestinal morphology and systemic immunity improved substantially: at 550 mg/L, jejunal villus height rose 63.5% and duodenal villus:crypt ratio from 8.67 to 11.16 (P < 0.05), while serum albumin, IgA, IgG, IgM, IL-6, IL-8 and TNF-α and antioxidant capacity (SOD, hydroxyl-radical inhibition) rose significantly (P < 0.05 to P < 0.01). The authors judged 550 mg/L optimal. ^[17] Measured drinking-water pH fell from 6.96 to 3.92 at that inclusion.

This matters practically for two reasons: water application reaches birds whose feed intake has collapsed (heat stress, coccidiosis challenge), and it sidesteps pelleting losses. The murine Salmonella work reaches the same conclusion — 0.1% in water outperformed 1% in feed. ^[22]

6. Practical inclusion rates and where the ceiling sits

Across species the effective band is narrower than most labels suggest. Broilers optimise at 2,000–6,000 mg/kg feed; weaned piglets need about 8,000 mg/kg for a measurable effect; late-lay hens at 10,000 mg/kg; fish at 3,000–4,500 mg/kg; drinking water at 550 mg/L. Every well-designed titration shows an inverted-U response, so exceeding the optimum costs money and can cost performance.

Table 10. Evidence-derived effective inclusion range by species, versus legally permitted limits

7. Regulatory status: European Union

Yes — and the 2001 entry point really was a zootechnical one. Commission Regulation (EC) No 1334/2001 provisionally authorised potassium diformate in the legal group "Growth promoters", making it the EU's first non-antibiotic growth promoter. That group no longer exists. As of today the only live EU zootechnical authorisation is Commission Implementing Regulation (EU) 2023/1698, for sows, at up to 12,000 mg/kg. Weaned-piglet and fattening-pig authorisations now sit in the technological category, which supports hygiene and process claims but not performance claims.

7.1 The 2001 growth-promoter authorisation — what it actually said

Commission Regulation (EC) No 1334/2001 of 2 July 2001 (OJ L 180, 3.7.2001, p. 18) authorised potassium diformate under Article 4 of Directive 70/524/EEC and, critically, listed it among the additives in Part II of Annex C — the group "Growth promoters". This is the zootechnical provision worth citing. ^[24]

Table 11. The 2001 EU authorisation as originally granted, then as consolidated on 16 April 2003

The recitals are worth quoting in customer dossiers: the Scientific Committee for Animal Nutrition delivered a favourable opinion on safety for animals, users, consumers and the environment under the conditions set out in the Annex. The increase to 1.8% for weaned piglets and 1.2% for fattening pigs in 2003 reflects the early tolerance and efficacy database built on exactly that species split. ^[24] The authorisation was tied to the person responsible for putting the additive into circulation, as Article 2(aaa) of Directive 70/524/EEC required for growth promoters — which is why later EU instruments name the authorisation holder explicitly.

7.2 What replaced it, and why the category change matters commercially

Regulation (EC) No 1831/2003 came into force in 2003 and abolished the "growth promoter" functional group for non-antibiotic products as such; existing authorisations had to be re-assessed and re-categorised. For KDF that produced a layered current position:

Table 12. Current EU authorisations for potassium diformate (position as of September 2026)

7.3 Cross-cutting conditions that apply regardless of entry

Regulation (EU) 2022/1374 imposes several conditions that formulators frequently miss: ^[26]

• Cumulative formic acid cap. Where different sources of formic acid are used together, total formic acid must not exceed 10,000 mg/kg complete feed in weaned piglets, pigs for fattening and sows.
• Cumulative KDF cap. The 6,000 / 12,000 mg/kg ceilings apply whether KDF comes from one source or several combined.
• Organic-acid stacking. Label declarations must state: "The simultaneous use of different organic acids or their salts is contraindicated where one or more of them is used at or near the maximum permitted content."
• Worker protection. EFSA classifies the additive as an eye irritant; operators must establish procedures and organisational controls, falling back on eye, skin and respiratory PPE where residual risk remains. ^[26],[28]
• Safe ceiling ratchet. In its 2022 opinion, the EFSA FEEDAP Panel explicitly reduced its maximum safe level for weaned piglets to 6,000 mg/kg and extended that conclusion to pigs for fattening, while retaining 12,000 mg/kg for sows. ^[28]

8. Regulatory status: United States

The United States has no equivalent of the EU zootechnical authorisation for potassium diformate. We could not identify any FDA new-animal-drug approval, FDA GRAS notice, or AAFCO Official Publication entry naming potassium diformate specifically in publicly accessible records as of September 2026 — notwithstanding widespread supplier marketing that asserts "GRAS" status. Confirm any US performance claim with regulatory counsel before use.

This is stated deliberately cautiously. Searches for a governing instrument return only supplier-authored marketing copy, which repeats the GRAS assertion without citing a docket number, notice number or AAFCO listing. Marketing repetition is not a citation, and we are not going to launder it into one here. What can be said defensibly:

• KDF is not an approved new animal drug, and the US does not operate an EU-style pre-market authorisation system for feed additives of this type. Products are ordinarily commercialised through GRAS self-determination for their intended technical effect, or through state-level AAFCO-recognised ingredient definitions.
• Long-standing GRAS and AAFCO standing exists for formic acid and several formate salts, but that standing does not automatically extend to the hydrogen-bonded dimer.
• Practical consequence: positioning KDF in the US as a processing aid, feed preservative or pH-control ingredient is materially different from positioning it as a growth promoter. The second framing carries claim risk on the US market in a way that it does not, for sows, in the EU.

9. Regulatory status: China

Potassium diformate has been an approved Chinese feed additive since 2005 and remains listed in the Feed Additive Catalogue. Ministerial Announcement No. 982 (12 January 2026) extended its approved scope to broiler chickens, with the function "improving feed conversion efficiency" and a recommended inclusion of 2–4 g/kg of complete feed on an 88% dry-matter basis. The recommended band sits squarely inside the trial-derived optimum.

Table 13. Chinese regulatory position for potassium diformate

The alignment between the Chinese recommended window (2,000–4,000 mg/kg) and the trial-derived optimum is commercially important and rare. Chart reviews place the broiler optimum between roughly 2,000 and 6,000 mg/kg; the two best-designed Chinese trials independently identified 2,000 mg/kg ^[10] and 6,000 mg/kg ^[12] as their optima from different directions, with 3,000 mg/kg emerging from the microbiology-led trial ^[15] and 5,000 mg/kg from the international comparison. ^[4] The officially recommended range covers the centre of that distribution.

10. Formulation and handling notes

KDF is hygroscopic and heat-sensitive, both of which are formulation rather than efficacy problems. Potassium formate systems contribute meaningfully to diet acid-binding-capacity reduction, but exceeding about 6,000 mg/kg in broilers or 8,000 mg/kg in piglets costs money without paying back. Handle it as an irritant dust, and keep it away from alkaline premix components.

• Moisture. The material is strongly hygroscopic; caking impairs flow but, unlike most active ingredients, caked product that is re-milled retains its activity. Store dry and use opened bags promptly. ^[7],[8]
• Heat. It is reported to remain reasonably stable through typical pelleting but decomposes at higher temperature, generating impurity and raising corrosiveness. Process literature routinely flags "high temperature easily decomposes" as its main handling weakness. ^[7],[8] Verify recovery analytically on your own line rather than assuming.
• Alkaline incompatibilities. Avoid co-mixing with sodium bicarbonate or other alkaline carriers; they neutralise the effect before it reaches the animal.
• Interaction with other organic acids. Do not stack KDF with benzoic acid, formic acid or their salts near the maximum permitted content; EU law requires the contraindication statement on the label. ^[26]
• Worker safety. EFSA classifies KDF as an eye irritant and, because data are absent, could not conclude on skin irritation or sensitisation. Operational controls come first; PPE including eye protection second. ^[26],[28]
• Acid-binding capacity. Diet buffering capacity — not simply stomach pH — drives how much acidifier is needed. Weaned starter diets are often above pH 5.8 and above ABC 30; the base data indicate weaned-piglet gastric pH only matures to adult levels (2.0–3.5) after about four months. ^[1],[2],[30]

11. Frequently asked questions

12. References

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18. Li J, Pan P. Effects of potassium diformate on laying performance, serum lipid metabolism indicators and hepatic lipid metabolism in laying hens during the late laying period [in Chinese]. China Feed. 2025;(18):9–12. doi:10.15906/j.cnki.cn11-2975/s.20251803
19. Jin C. Application of potassium diformate and the Bacillaceae bacteria isolated from the soil of Illicium verum plantation in diets of laying hens [master's thesis, in Chinese]. Shandong Agricultural University; 2022.
20. Xue X. Effect of potassium diformate in diet on growth performance, digestion and absorption capacity and intestinal barrier function of juvenile grass carp (Ctenopharyngodon idella) [master's thesis, in Chinese]. Sichuan Agricultural University; 2023.
21. Chai Q. Effects of dietary diformate potassium supplementation on immune function of juvenile grass carp [master's thesis, in Chinese]. Sichuan Agricultural University; 2023.
22. Sun Y, Yu P, Chen H, Tan Y, Chen X, Zhang T, Gao T, Zhou R, Li L. Evaluation of the efficacy of potassium diformate in the prevention of Salmonella infection and the effect on intestinal flora [in Chinese]. Acta Veterinaria et Zootechnica Sinica. 2023;54(5):2101–2113. doi:10.11843/j.issn.0366-6964.2023.05.031
23. Shangguan M, Li Y, Dang W, Zhan H, Cao L, Fan A, Ren K. Effects of benzoic acid and potassium diformate on growth performance, gastrointestinal pH and nutrient apparent digestibility of Rex rabbits [in Chinese]. Chinese Journal of Animal Science. Advance online publication 27 October 2023. doi:10.19556/j.0258-7033.20221209-05
24. Commission Regulation (EC) No 1334/2001 of 2 July 2001 concerning the provisional authorisation of a new additive in feedingstuffs. Official Journal of the European Communities L 180, 3.7.2001, p. 18. Consolidated text available via ELI: data.europa.eu/eli/reg/2001/1334/2003-04-16
25. Commission Implementing Regulation (EU) 2021/2092 concerning the authorisation of potassium diformate as a feed additive for weaned piglets and pigs for fattening. Authorisation valid until 20 December 2031; maximum content 6,000 mg/kg complete feedingstuff at 12% moisture.
26. Commission Implementing Regulation (EU) 2022/1374 of 5 August 2022 concerning the authorisation of potassium diformate as a feed additive for weaned piglets, pigs for fattening and sows, and repealing Implementing Regulation (EU) No 333/2012. Official Journal of the European Union L 206, 8.8.2022, pp. 35–37. ELI: data.europa.eu/eli/reg_impl/2022/1374/oj
27. Commission Implementing Regulation (EU) 2023/1698 of 6 September 2023 concerning the renewal of the authorisation of a preparation of potassium diformate as a feed additive for sows and repealing Regulation (EU) No 104/2010. In force 20 September 2023; maximum content 12,000 mg/kg complete feedingstuff at 12% moisture.
28. EFSA Panel on Additives and Products or Substances used in Animal Feed (FEEDAP). Assessment of the feed additive consisting of potassium diformate for all animal species for the renewal of its authorisation. EFSA Journal. 2022;20(3):7167.
29. Ministry of Agriculture and Rural Affairs of the People's Republic of China. Announcement No. 982 — approval of seven new feed additive varieties and extension of the approved scope of eight feed additive varieties. Published 12 January 2026.
30. Product technical dossier and internal feeding trial records. Company data, not peer-reviewed — see Appendix.

13. Appendix: internal product data (not peer-reviewed)