Veltassa is indicated for the treatment of hyperkalaemia in adults.

Posology

Initiation of therapy

The recommended starting dose is at least 8.4 g of patiromer once a day.
In general, administration of Veltassa should be separated by 3 hours from other oral medicinal
products. Separation is not needed for certain medicinal products (see section 4.5).
Because of delayed onset of action, Veltassa should not replace emergency treatment for
life-threatening hyperkalaemia.

Dosage adjustment and maintenance therapy

The daily dose of Veltassa should be adjusted based on potassium level and desired target
range. The daily dose may be increased or decreased by intervals of one week in increments of
8.4 g as needed to reach the desired target range, up to a maximum daily dose of 25.2 g.
Multiple sachets may be used to achieve the desired dose. If the potassium level falls below the
desired target range, administration of Veltassa should be reduced or discontinued.
If a dose of Veltassa is forgotten, the forgotten dose should be taken as soon as possible on the
same day. The forgotten dose should not be taken with the following dose.

Method of administration

Oral use.

Veltassa should be mixed with water or other fluids or soft foods listed below until a uniform
consistency is achieved, according to the following steps:

The entire dose of Veltassa should be first mixed with approximately 40 mL of water
(3 tablespoons) in a glass. Then add approximately 40 mL of water and carefully mix the
suspension. The powder will not dissolve. If necessary, water can be added to the mixture to
obtain the desired consistency.

The mixture should be consumed immediately. If powder remains in the glass after consuming
the mixture, add water, mix and drink immediately. Repeat if necessary to guarantee
administration of the entire dose.

The following liquids or soft foods can be used instead of water to prepare the mixture by
following the same steps as described above: apple juice, cranberry juice, pineapple juice,
orange juice, grape juice, pear juice, apricot nectar, peach nectar, yoghurt, milk, thickener, apple
sauce, vanilla and chocolate pudding.

The potassium content of liquids or soft foods used to prepare the mixture should be considered
as part of the dietary recommendations on potassium intake for each individual patient.

Veltassa can be taken with or without food. Veltassa should not be heated (for example in a
microwave) or added to hot food or beverages. Veltassa should not be taken in its dry form.

Special dosing instructions

Dialysis patients

There is only limited data available on the use of Veltassa in dialysis patients. No specific
guidelines for dose and administration were applied to these six patients during clinical studies.

Elderly patients

Among the total number of patients treated with Veltassa during clinical trials, 1,307 (61.2%)
patients were 65 years and older, and of these patients, 500 (23.4%) were 75 years and older. No
specific dose guidelines were applied in these patients during these studies.

Children and adolescents

The safety and efficacy of Veltassa in children and adolescents aged up to 18 years have not yet
been established. No data are available.

Hypomagnesaemia

Patiromer may cause hypomagnesaemia by binding magnesium in the colon. In clinical studies,
magnesium levels <1.4 mg/dL were observed in 7.1% of patients treated with Veltassa, with
0.3% of patients developing magnesium levels <1.0 mg/dL. Mean reductions in magnesium
level occurred at the start of treatment with Veltassa and were ≤0.118 mg/dL one week after the
start of treatment with Veltassa. Magnesium levels must be monitored for one month after

initiating treatment with Veltassa and monitoring should be continued in the event of decreased
serum levels of magnesium. Magnesium supplementation should be planned in patients who
develop hypomagnesaemia during treatment with Veltassa.

Gastrointestinal disorders

Patients with a history of intestinal blockage or major digestive surgery, diabetic gastroparesis,
presenting severe gastrointestinal disorders or swallowing disorders were not included in the
clinical studies. Treatment with Veltassa should be avoided in these patients.

Discontinuation of treatment with Veltassa

Potassium levels may increase upon discontinuation of treatment with Veltassa, particularly in
cases where treatment is followed by a renin angiotensin aldosterone system (RAAS) inhibitor.
Patients should be informed that they must not discontinue treatment without consulting their
doctor. Increases in potassium level may occur starting from the 2nd day after the last dose of
Veltassa.

Serum potassium levels

Serum potassium should be monitored when clinically indicated, including after changes are
made to medicinal products that affect the serum potassium concentration (e.g. RAAS inhibitors
or diuretics) and after the Veltassa dose is titrated.

Sorbitol

Veltassa contains sorbitol as part of the counterion complex. The sorbitol content is
approximately 4 g (10.4 kcal) per 8.4 g of patiromer. Patients presenting a hereditary intolerance
to fructose (HFI) must not take/recieve this medicinal product.

Fluoride

Veltassa contains fluoride. In patients presenting severe chronic renal insufficiency (CRI), all
other sources of fluoride should be limited.

Information about calcium

Veltassa contains calcium as part of the counterion complex. Calcium is partially released some
of which may be absorbed (see section 5.1). However, in clinical studies with durations up to
one year, no meaningful changes in mean serum calcium levels were observed. The benefits and
risks of administering this medicinal product should be carefully evaluated by the physician in
at risk patients.

Veltassa has the potential to bind certain medicinal products co-administered by oral route,
which may reduce their gastrointestinal absorption. As patiromer is not absorbed or metabolised
by the body, there are limited effects on the function of other medicinal products.

Table 1 shows the medicinal products tested for interactions with Veltassa and
recommendations for administration of these medicinal products with Veltassa. For oral
medicinal products not listed, administration of patiromer should be separated by at least 3
hours as precautionary measure.

Effect of Food on Veltassa

In an open-label study, 114 patients with hyperkalaemia were randomized to patiromer once
daily with food or without food. Serum potassium at the end of treatment, the change from
baseline in serum potassium, and the mean dose of patiromer were similar between groups.

Pregnancy

To date, there are no clinical data regarding the use of Veltassa in pregnant women.
Animal studies have not shown any direct or indirect toxicity affecting pregnancy, embryonic
development, foetal development and/or postnatal development (see section 5.3).
As a precautionary measure, it is preferable to avoid the use of Veltassa during pregnancy.

Breastfeeding

No effect on the breastfeeding newborn infant is expected since the systemic exposure to
patiromer in breastfeeding woman is negligible. A decision must be made whether to
discontinue breastfeeding or to discontinue/abstain from patiromer therapy taking into account
the benefit of breastfeeding for the child and the benefit of therapy for the woman.

Fertility

There are no data on the effect of patiromer on fertility in humans. Animal studies showed no
effects on reproductive function or fertility (see section 5.3).

Veltassa has no or negligible influence on the ability to drive and use machines.

Summary of the safety profile

Veltassa’s safety profile is based on a total of 2,135 patients having participated in clinical
studies and on post-marketing experience.
The majority of the adverse reactions (AR) reported were hypomagnaesemia and
gastrointestinal disorders, with the most frequently reported ARs being: constipation, diarrhoea,
abdominal pain, nausea, flatulence, vomiting and hypersensitivity. Gastrointestinal disorders
were generally of a mild to moderate intensity, did not appear to be dose-dependent, generally
resolved spontaneously or with treatment and none were described as serious. The
hypersensitivity reactions included skin rashes, urticaria, swelling in the oral cavity and on the
lips, and were mild to moderate.
Note: Diarrhoea is an umbrella term for diarrhoea and frequent defaecation. Abdominal pain is
an umbrella term encompassing the preferred terms of abdominal complaints, abdominal pain
and upper abdominal pain. Constipation is an umbrella term encompassing the preferred terms
of constipation and hard stools.

Tabulated list of adverse reactions

Adverse reactions are listed below by system organ class and by frequency.
Frequencies of undesirable effects: very common (≥1/10), common (≥1/100 to <1/10),
uncommon (≥1/1,000 to <1/100), rare (≥1/10,000 to <1/1,000), very rare (<1/10,000), not
known (cannot be estimated from the available data). Within each frequency grouping,
undesirable effects are presented in order of decreasing seriousness.

Doses of Veltassa greater than 50.4 g of patiromer per day have not been studied. As excessive
doses of Veltassa may cause hypokalaemia, serum potassium levels must be monitored. If
medical proves necessary, appropriate measures to re-establish normal potassium levels should
be undertaken.

Pharmacotherapeutic group: Drugs for treatment of hyperkalaemia and hyperphosphataemia.
ATC code: V03AE09

Mechanism of action
Veltassa is a non-absorbed, cation exchange polymer that contains a calcium-sorbitol complex
as a counterion.
Veltassa increases faecal potassium excretion through binding of potassium in the lumen of the
gastrointestinal tract. The binding of potassium reduces the concentration of free potassium in
the gastrointestinal lumen, which results in a reduction of serum potassium levels.

Pharmacodynamics

It has been shown that Veltassa binds potassium in vitro and in vivo in experimental animal
models.
In a phase 1 study conducted in healthy adult volunteers (6-8 subjects per group), Veltassa
(from 0 g to 50.4 g of patiromer daily) administered three times daily for 8 days induced a
dose-dependent increase in faecal excretion of potassium. A corresponding dose-dependent
decrease in kaliuresis without effect on serum potassium was also observed. Compared to
placebo, Veltassa at doses of 25.2 g and 50.4 g daily significantly reduced mean daily kaliuresis.
In a phase 1, open label, repeat dose crossover study conducted among 12 healthy volunteers,
the dose of 25.2 g of patiromer daily was orally administered following a schedule of once
a day, twice a day or three times a day for 6 days according to a randomly assigned sequence.
A significant increase in mean daily faecal excretion of potassium and a concomitant decrease
in mean daily kaliuresis was observed with the three dosing schedules. The mean increase in
faecal excretion of potassium was from 1,283 to 1,550 mg/day and mean decrease in kaliuresis
was from 1,438 to 1,534 mg/day across the three dosage schedules. No significant difference
was observed between the dosing schedules in terms of mean daily faecal and urinary excretion
of potassium, either in the global comparison or paired comparison. Daily urinary excretion of
calcium increased by 53 mg/day, 66 mg/day and 73 mg/day compared to baseline with the
schedules once daily, twice daily and three times daily, respectively.

In a non-controlled, open-label study, 25 patients presenting with hyperkalaemia (mean baseline
potassium level of 5.9 mEq/L) and chronic renal insufficiency followed a controlled potassium
regimen for three days, then received 16.8 g of patiromer per day (in two fractionated doses) for
two days, while continuing the controlled regimen. A statistically significant reduction in
potassium levels (0.2 mEq/L) was observed 7 hours after the initial dose. Potassium levels
continued to decline during the 48-hour treatment period (0.8 mEq/L 48 hours after initial dose).
Potassium levels remained stable for 24 hours following the last dose, then increased during the
4-day observation period following discontinuation of Veltassa.

* The full circle indicates the time at which the first statistically significant reduction was
identified. A mean reduction of 0.8 mEq/L was observed at hour 48 (p <0.001).

Comments: hours 72 to 0 = pre-screening period with controlled potassium regimen; hours 0 to
58 = period of treatment with Veltassa 16.8 g per day in fractionated doses in a hospital
environment; hour 58 to day 6 = period of outpatient follow-up.

Clinical efficacy and safety

The potassium-lowering effect of patiromer has been proven in 5 clinical studies with the
participation of patients with hyperkalaemia or normokalaemic patients who received RAASi
inhibitors and thus were at an increased risk of hyperkalaemia. The effect of patiromer on
hyperkalaemic patients with chronic renal disease who received RAASi inhibitors was
examined in a single-blind study with subsequent randomised withdrawal part. An open 52-
week study was conducted with hyperkalaemic patients with chronic kidney disease,
uncontrolled high blood pressure and type 2 diabetes mellitus who received RAASi inhibitors.
In two randomised, double-blind, placebo-controlled studies, patiromer was examined on
normokalaemic patients with heart failure or chronic kidney disease and resistant high blood
pressure, or during simultaneous start of treatment with RAASi inhibitors (spironolactone). In a
double-blind, placebo-controlled study, patients with heart failure and reduced ejection fraction
were included who had hyperkalaemia or recently occurring hyperkalaemia and who were able
to use and maintain the approved doses of RAASi inhibitors and to achieve or maintain
normokalaemia during patiromer intake. Afterwards, the effect of patiromer on the serum
potassium level was examined in a randomised withdrawal procedure.
Overall, the 5 studies included 1,918 participating patients who received at least one dose of
patiromer. Of these, 64.6% suffered from chronic kidney disease with an eGFR of <6
mL/min/1.73 m2, and 54.3% from diabetes mellitus and 77.9% from heart failure.

Study 1 (OPAL-HK)

Randomised, single-blind, two-part withdrawal study in patients with chronic renal
insufficiency (CRI) and hyperkalaemia receiving stable doses of at least one RAAS inhibitor.

The safety and efficacy of Veltassa have been demonstrated in a randomised, single blind, two
part withdrawal study evaluating Veltassa in patients presenting CRI and hyperkalaemia,
receiving stable doses of at least one RAAS inhibitor (i.e. angiotensin converting enzyme inhibitor [ACEI], angiotensin II receptor blocker [ARB] or mineralocorticoid receptor
antagonists [MRA]).
In part A, 243 patients were treated with Veltassa for 4 weeks. The initial dose of Veltassa was
8.4 g of patiromer daily (in fractionated doses) in patients with a potassium level from
5.1 mEq/L to <5.5 mEq/L (mmol/L) at baseline and 16.8 g of patiromer daily (in fractionated
doses) in those with a potassium level from 5.5 mEq/L to <6.5 mEq/L at baseline. The dose was
adjusted, as needed, on the basis of potassium level, determined starting from day 3 and then in
bi-weekly visits (weeks 1, 2 and 3) to the end of the 4-week treatment period, for the purpose of
maintaining potassium level within the target range (3.8 mEq/L to <5.1 mEq/L).

Mean patient age was 64 years, 58% of patients were male and 98% were of Caucasian origin.
Approximately 97% of patients presented with hypertension, 57% with type 2 diabetes and 42%
with heart failure.

Mean daily doses of Veltassa were 13 g and 21 g in patients with potassium levels of 5.1 to
<5.5 mEq/L and 5.5 to <6.5 mEq/L, respectively.

Mean potassium level was 5.58 mEq/L at baseline and the mean variation (SD) of potassium
level between the baseline visit and week 4 of part A was 1.01 (0.031) mEq/L, 95% CI: [-1.07; -
0.95] (see figure 2). This mean reduction of potassium level was statistically significant. For
the secondary endpoint of part A, 76% (95% CI: 70%, 81%) of patients had a potassium level in
the target range of 3.8 mEq/L to <5.1 mEq/L at week 4 of part A.

In Part B, 107 patients who had potassium levels from 5.5 mEq/L to <6.5 mEq/L at the baseline
visit in part A, and whose potassium levels were within the target range (3.8 mEq/L to
<5.1 mEq/L) at week 4 of part A and who were still receiving one or more RAAS inhibitors
were randomised to continue treatment with Veltassa or to receive placebo for 8 weeks in order
to evaluate the effect of discontinuing Veltassa on potassium levels. In the patients in the
Veltassa group, the mean daily dose was 21 g at the start and during part B.
The primary endpoint in part B was the variation in potassium level from inclusion in part B
until the first visit during which the patient’s potassium level for the first time fell outside of the

range of 3.8 to <5.5 mEq/L or until week 4, if the patient’s potassium level remained in this
range. In part B, potassium levels increased by 0.72 mEq/L, 95%CI [0.46, 0.99] in patients
receiving placebo, while showing no change in patients continuing treatment with Veltassa.
The percentage of patients having presented a serum potassium level ≥5.1 mEq/L at any point in
part B was higher in the group receiving placebo (91% [95% CI: 83%, 99%]) than in the group
treated with patiromer (43% [95% CI: 30%, 56%]). The percentage of patients having presented
a potassium level ≥ 5.1 mEq/L at any point in part B was higher in the group receiving placebo
(60% [95% CI: 47%, 74%]) than in the group treated with patiromer (15% [95% CI: 6%, 24%]).
Fifty two percent (52%) of patients receiving placebo needed to discontinue treatment with a
RAAS inhibitor because of reoccurrence of hyperkalaemia versus 5% of patients treated with
Veltassa.

Study 2 (AMETHYST-DN)

The effect of treatment with Veltassa for a duration of up to 52 weeks was evaluated in an open
label study of 304 hyperkalaemic patients with CRI and type 2 diabetes on stable doses of a
RAAS inhibitor. Reductions in potassium levels observed during treatment with Veltassa were
maintained for one year with regular treatment. In patients with a baseline potassium level of
>5.0 to 5.5 mEq/L having already received an initial dose of 8.4 g patiromer per day (in
fractionated doses), the mean daily dose was 14 g. In those with a baseline potassium level of
>5.5 to <6.0 mEq/L having already received an initial dose of 16.8 g patiromer per day (in
fractionated doses), the mean daily dose was 20 g during the entire study.

Study 3 (PEARL-HF)

The ability of patiromer to enable concomitant spironolactone treatment was investigated in
a randomised, double-blind, placebo-controlled study in heart failure patients who were

clinically indicated to receive MRA. Patients initiated spironolactone at 25 mg/day at the same
time as their randomised treatment (patiromer 12.6 g BID or placebo), and were up-titrated to
50 mg/day after Day 14 if serum potassium was >3.5 and ≤5.1 mEq/L. Of the 105 patients who
were randomised and received study treatment (patiromer 56; placebo 49), mean age was
68.3 years, 60.6% were men, 97.1% were Caucasian, and mean eGFR was 81.3 mL/min. Mean
baseline serum potassium values were 4.71 mEq/L for patiromer and 4.68 mEq/L for placebo.
The primary efficacy endpoint, change from baseline in serum potassium to the end of the 28-
day treatment period, was significantly lower (p<0.001) in the patiromer group (LS mean
[SEM]: -0. 21 [0.07] mEq/L) as compared to the placebo group (LS mean [SEM]: +0.23 [0.07]
mEq/L). There were also fewer patients in the patiromer group with serum potassium values
>5.5 mEq/L (7.3% vs. 24.5%; p=0.027) and more patients on spironolactone 50 mg/day (90.9%
versus 73.5%, p=0.022).

Study 4 (AMBER)

Another randomised, double-blind, placebo-controlled study investigated the effect of patiromer
on the tolerability of spironolactone treatment in patients with treatment-resistant hypertension
and CRI. During the study, patients were randomised to receive patiromer or placebo in addition
to spironolactone (25 mg/day; increased to 50 mg/day from week 3 in patients with a systolic
blood pressure ≥120 mmHg and a serum potassium of ≤5.1 mEq/L). To maintain a serum
potassium level of between ≥4.0 mEq/L and ≤5.1 mEq/L, the patiromer/placebo dose could be
increased on a weekly basis from the starting dose of 8.4 g/day to a maximum of 25.2 g/day.
A total of the 295 randomized patients (147 receiving patiromer; 148 receiving placebo) with a
mean age of 68.1 years and a mean eGFR of 35.73 mL/min/1.73m2 were randomised, stratified
according to baseline serum potassium levels (mean serum potassium was 4.71 mEq/L in the
patiromer arm and 4.68 mEq/L in the placebo control arm) and a history of diabetes mellitus
(type 1 or type 2). The primary endpoint was the percentage of patients who continued
spironolactone treatment until the end of the study (12 weeks). This percentage was
significantly greater in the patiromer group than in the placebo group (85.7% versus 66.2%;
p <0.0001). Patients in the patiromer arm received a spironolactone dose of 50 mg/day more
often (69.4% versus 51.4% in the placebo control arm) and their serum potassium levels were
≥5.5 mEq/L less often than patients in the placebo control arm (35.4% vs 64.2% in the placebo
control; p < 0.001).

Study 5 (DIAMOND)

The effects of patiromer on serum potassium were examined in a double-blind, placebocontrolled,
randomised-withdrawal, parallel-group study on patients who received the doses of
RAASi inhibitors approved for the treatment of heart failure and maintained or achieved
normokalaemia during the administration of patiromer. Before randomisation, the patients were
either hyperkalaemic while they received RAASi inhibitors or normokalaemic with a history of
hyperkalaemia during the intake of RAASi inhibitors in the preceding 12 months, which led to a
decrease of the dose of RAASi inhibitors or to withdrawal from RAASi inhibitors. In all
patients, patiromer was started at a dose of 8.4 g per day and titrated weekly up to a maximum
dose of 25.2 g per day in order to maintain the serum potassium level of ≥4.0 mEq/L and ≤5.0
mEq/L. Hyperkalaemic patients received patiromer from the start; normokalaemic patients
received patiromer in week 1 or later. In parallel to this, the medication with the RAASi
inhibitor was optimised, including the start, dose escalation and maintenance of at least 50% of
the prescribed ACEi/ARB/ARNI target doses and 100% of the prescribed MRA target doses. As
soon as these RAASi inhibitor target doses were achieved and the patients showed stable serum
potassium levels of ≥4.0 mEq/L and ≤5.0 mEq/L for at least one week, they were randomised to
either patiromer or placebo.

Of the 1,168 patients in whom patiromer was started, 130 did not complete the run-in part. Of
the 1,038 patients who did complete the run-in part, 878 (85%) were randomised (patiromer:
439, placebo: 439). The mean age of randomised patients was 66.9 years; 72.9% were men,
97.9% Caucasian, and the mean eGFR was 63.0 mL/min/1.73 m2. At the time of randomisation,
the mean baseline serum potassium value was 4.72 mEq/L.

All participants had a history of hyperkalaemia. At the start of the study, a total of 40.3% of the
participants were hyperkalaemic and 59.7% were normokalaemic but had a history of
hyperkalaemia in the preceding 12 months.

The primary efficacy endpoint was the difference between the adjusted mean change (standard
error [SE]) of the serum potassium level from the baseline, which was analysed with a mixed
model for repeated measures (MMRM). The difference of the adjusted mean changes compared
to the baseline was 0.097 mEq/L (95% CI: –0.128; –0.067). The mean change in serum K+
from the baseline value was statistically significantly lower in the patiromer group (0.029
[0.019] mEq/L) (p 0.001) than in the placebo group (0.127 [0.019] mEq/L).
The time until the first hyperkalaemia event (defined as serum potassium level > 5.5 mEq/L)
was significantly shorter for patiromer compared to placebo (p = 0.006), with a hazard ratio of
0.63 (95% CI: 0.45; 0.87).

The proportion of patients in whom the MRA medication (spironolactone or eplerenone) was
reduced under the target dose was 13.9% in the patiromer group compared to 18.9% in the
placebo group. The hazard ratio for the time until the first MRA dose reduction of patiromer
compared to placebo was 0.62 (95% CI: 0.45; 0.87), and the treatment difference was
statistically significant (p = 0.006).

In the pre-defined subgroups of eGFR </≥ 60 mL/min/1.73 m2, </≥ 45 mL/min/1.73 m2 with
post-hoc analysis of eGFR </≥ 30 mL/min/1,73 m2, patiromer allowed to use effective RAAS
inhibitor doses, controlled serum K+ and minimised the risk of hyperkalaemia in patients with
HFrEF and mild to severe chronic renal disease.

Overall, 31.2% of the patients in the patiromer group and 45.1% of the patients in the placebo
group had at least one hyperkalaemia event with a serum potassium value of > 5.5 mEq/L
reported by the investigator. The annualised event rate ratio for patiromer was 0.658 compared
to placebo (95 CI%: 0.534; 0.810) , which was statistically significant (p < 0.001).

An unadjusted win-ratio approach was used for the two hierarchically tested secondary
endpoints: one approach for which complex hyperkalaemia-dependent hard endpoints were
used, including death from a cardiovascular cause, hospital stays due to cardiovascular diseases
and three grades of hyperkalaemia events, showing a win ratio of 1.526 (95% CI: 1.231; 1.906;
p < 0.001), which favours treatment with patiromer; and one in which a new score was used for
the application of RAASi inhibitors (0–8 points), showing a good rate of achieving a high score
for the application of RAASi inhibitors in patients treated with patiromer compared to the
placebo group, with a win ratio of 1.4248 (95% CI: 1.003; 1.564; p = 0.048)

Absorption
Patiromer works by binding potassium in the gastrointestinal tract. Serum concentration is
therefore not relevant for its efficacy. Because of the insolubility and non-absorption
characteristics of Veltassa, many classic pharmacokinetic studies have not been possible to
conduct.
In ADME (absorption, distribution, metabolism and excretion) studies with radiolabelling
conducted in rats and dogs, patiromer was not systemically absorbed.

Distribution
Quantitative whole-body autoradiography analysis in rats demonstrated that radioactivity was
limited to the gastrointestinal tract, with no detectable level of radioactivity in any other tissues
or organs.

Biotransformation
Not applicable, because of Veltassa’s insolubility and non-absorption characteristics.

Elimination
In ADME studies with radiolabelling in rats and dogs, patiromer was excreted through the
faeces.

Non-clinical data reveal no special hazard for humans based on conventional studies of safety
pharmacology, repeated dose toxicity, genotoxicity, toxicity to reproduction and development.
Patiromer did not demonstrate genotoxic effects in the reverse mutation studies (Ames test),
chromosomal or micronucleus aberrations in rats.

No carcinogenicity studies have been conducted.

Patiromer had no negative impact on fertility in male or female rats at doses of up to 10 times
the recommended maximum daily dose in humans (RMDH). Patiromer did not have any
harmful effects on embryonic or foetal development, either, when administered to pregnant rats
at doses of up to 6 g/kg, thus providing a margin of exposure 12 times greater than the RMDH
and administered to pregnant rabbits at doses of up to 3 g/kg, thus providing a margin of
exposure 6 times greater than the RMDH.

Xanthan gum

Not applicable.

Store and transport refrigerated (2°C – 8°C). Avoid any exposure to temperatures above 40°C.
Once issued to the patient, Veltassa can be kept at room temperature (below 25°C) for a
maximum of 6 months.
Do not use Veltassa after the expiry date printed on the sachet.

The mixture should be taken within 1 hour of initial suspension.
Keep out of the sight and reach of children.

8.4 g, 16.8 g or 25.2 g of patiromer (as patiromer sorbitol calcium (patiromer sorbitex calcium)),
as powder in sachets made of five layers: polyethylene, aluminium, polyethylene, polyester and
paper.

Pack sizes: box of 30 sachets.

Not all strengths may be marketed.

Any unused medicinal product or waste material should be disposed of in accordance with local
requirements.