Sanofi’s broad range of resources continue to build on the knowledge within lysosomal storage disorders and empower the rare disease community by supporting professional bodies and HCPs with a variety of resources and initiatives across the four disease areas; Fabry, Gaucher, MPS I and Pompe. As a result, we have helped to contribute to the increased chances of early diagnosis and improved treatment plans. Watch this video to find out more about our continued commitment to support professionals in our shared goal for Better Care for Rare.

<h2>Supporting experts in rare disease</h2>
See how Sanofi continues to assist professional bodies and healthcare professionals in the field of rare disease.

BETTER-CARE-FOR-RARE

RARE-DISEASE

Supporting the rare disease community

This is intended for HCPs practising in Great Britain (England, Scotland, Wales) only.
In this video, find out how we used glycoengineering and chemical conjugation to help overcome the challenge of cellular delivery of acid alpha-glucosidase, by increasing the levels of bis-M6P1,4&nbsp;compared to Myozyme (alglucosidase alfa).

POMPE

Why we developed Nexviadyme®▼ (avalglucosidase alfa)

Nexviadyme® (avalglucosidase alfa) prescribing information GB

Myozyme® (alglucosidase alfa) prescribing information GB

Find out how we have led with science for over 30 years,5&nbsp;and continue to bring innovation to people living with lysosomal storage disorders.

Watch how we used preclinical mice models of Pompe to design Nexviadyme&reg;, and improve maintenance of muscle strength compared to Myozyme&reg;.1,3

 Nexviadyme®▼(avalglucosidase alfa) prescribing information GB

Myozyme® (alglucosidase alfa) prescribing information GB

Myozyme® (alglucosidase alfa) prescribing information NI

<a href="${link:{uuid:{55f30477-c7e2-49c0-8cfc-16966f28d4c2},repository:{dam},path:{/Portal/UK/Prescribing-links/Praluent-PI-GB-October-2022.pdf}}}" target="_blank">Prescribing Information(GB)</a>

<a href="${link:{uuid:{9e0d6f97-2ebb-4422-92ab-569b89c7dfe0},repository:{dam},path:{/Portal/UK/Prescribing-links/Praluent-PI-NI.pdf}}}" target="_blank">Prescribing Information(NI)</a>

ODYSSEY FH I and FH II: 78 week results with alirocumab treatment in 735 patients with heterozygous familial hypercholesterolaemia.
Kastelein JJP, et al. Eur Heart J 2015; 36:2996–3003.
All of the information and data within this section (unless noted) is a summary of this publication.
<ul>
</ul>

<h2>Study objectives</h2>
The ODYSSEY FHI and FH II studies evaluated the long-term efficacy and safety of Praluent®&nbsp;75/150 mg in heterozygous familial hypercholesterolaemia‡ (HeFH) patients with inadequately controlled low-density lipoprotein cholesterol (LDL-C) despite maximally tolerated dose (MTD) statins** ± other lipid-lowering therapies (LLTs).
<ul>
</ul>

<h2>Study design</h2>
ODYSSEY FH I and FH II studies had similar study designs with FH I performed at 89 sites across North America, Europe and South Africa whilst FH II was performed across 26 sites in Europe.
Both FH I and FH II were 78 week, multicentre, double-blind, placebo-controlled, parallel group, phase III studies involving 735 adult HeFH‡ patients (FH I, n=486; FH II, n=249) who were receiving MTD statins** ± other LLTs with:
<ul>
 <li>LDL-C ≥1.8 mmol/L in patients with prior cardiovascular events†</li>
</ul>
or
<ul>
 <li>LDL-C ≥2.6 mmol/L in patients without a history of CV events</li>
</ul>
Patients were randomised to subcutaneous Praluent®&nbsp;75 mg every 2 weeks (Q2W) (FH I, n=323; FH II, n=167) or placebo Q2W (FH I, n=163; FH II, n=82) (Figure 1). Praluent®&nbsp;dose was increased to 150 mg Q2W at Week 12 if Week 8 LDL-C was ≥1.8 mmol/L.
The primary efficacy endpoint was the percentage change in LDL-C from baseline to Week 24. Secondary endpoints included:
<ul>
 <li>Proportion patients achieving the pre-specified LDL-C level target of &lt;1.8 mmol/L at Week 24</li>
 <li>Percentage change in LDL-C from baseline to Week 78</li>
 <li>Safety - including incidence of treatment-emergent adverse events (TEAEs), treatment-emergent serious AEs (SAEs), injection site reactions and adjudicated CV events.</li>
</ul>

Figure 1: ODYSSEY FHI and FH II: Study design&nbsp;- Adapted from Kastelein JJP, et al. Eur Heart J 2015; 36:2996–30031

<h3>Baseline characteristics</h3>
Baseline characteristics were well balanced between the treatment groups (Table 1). In FH I and FH II, 85.8% and 91.6% of Praluent patients received study treatment for ≥76 weeks versus 87.7% and 90.1% of placebo.

<table cellpadding="20" style="width:100%;">
 <tbody>
 <tr>
 <td colspan="1" rowspan="2" style="background-color: rgb(0, 155, 195); width: 40%;">
 &nbsp;
 &nbsp;</td>
 <td style="background-color:#009bc3">
 Praluent 
 75/150 mg 
 (n=323)</td>
 <td style="background-color:#009bc3">
 Placebo 
 (n=163)</td>
 <td style="background-color:#009bc3">
 Praluent 
 75/150 mg 
 (n=167)</td>
 <td style="background-color:#009bc3">Placebo 
 (n=82)</td>
 </tr>
 <tr>
 <td colspan="2" rowspan="1" style="background-color:#009bc3">
 FH I</td>
 <td colspan="2" rowspan="1" style="background-color:#009bc3">
 FH II</td>
 </tr>
 <tr>
 <td colspan="5">
 Demographics</td>
 </tr>
 <tr>
 <td>
 Age in years, mean ±SD</td>
 <td>
 52.1 ± 12.9</td>
 <td>
 51.7 ± 12.3</td>
 <td>
 53.2 ± 12.9</td>
 <td>
 53.2 ± 12.5</td>
 </tr>
 <tr>
 <td>
 Male, %</td>
 <td>
 55.7</td>
 <td>
 57.7</td>
 <td>
 51.5</td>
 <td>
 54.9</td>
 </tr>
 <tr>
 <td colspan="5">
 CV history/risk factors</td>
 </tr>
 <tr>
 <td>
 CHD history*, %</td>
 <td>
 45.5</td>
 <td>
 47.9</td>
 <td>
 34.7</td>
 <td>
 37.8</td>
 </tr>
 <tr>
 <td>
 CHD risk&nbsp;equivalent†, %</td>
 <td>
 16.7</td>
 <td>
 15.3</td>
 <td>
 9.0</td>
 <td>
 4.9</td>
 </tr>
 <tr>
 <td>
 Type 2 diabetes, %</td>
 <td>
 9.9</td>
 <td>
 15.3</td>
 <td>
 4.2</td>
 <td>
 3.7</td>
 </tr>
 <tr>
 <td colspan="5">
 Lipid medication</td>
 </tr>
 <tr>
 <td>
 Any statin, %</td>
 <td>
 100</td>
 <td>
 100</td>
 <td>
 100</td>
 <td>
 100</td>
 </tr>
 <tr>
 <td>
 High dose statin§, %</td>
 <td>
 82.7</td>
 <td>
 85.3</td>
 <td>
 86.8</td>
 <td>
 91.5</td>
 </tr>
 <tr>
 <td>
 Ezetimibe, %</td>
 <td>
 56.0</td>
 <td>
 59.5</td>
 <td>
 67.1</td>
 <td>
 64.6</td>
 </tr>
 <tr>
 <td colspan="5">
 Lipid parameters</td>
 </tr>
 <tr>
 <td>
 LDL-C, (calculated) mmol/L ± SD</td>
 <td>
 3.7 ± 0.1</td>
 <td>
 3.7 ± 0.1</td>
 <td>
 3.5 ± 0.1</td>
 <td>
 3.5 ± 0.1</td>
 </tr>
 </tbody>
</table>

HD = coronary heart disease; CV = cardiovascular; LLT = lipid-lowering therapy, SD= standard deviation. *CHD history defined as acute myocardial infarction, silent myocardial infarction, unstable angina, or coronary revascularization. †CHD risk equivalent; Ischaemic stroke, peripheral arterial disease, moderate chronic kidney disease (estimated glomerular filtration rate of ≥30 and ≤60 mL/min/1.73 m2), and diabetes with two or more risk factors. §High-dose statin therapy defined as daily doses of 40–80 mg atorvastatin, 20–40 mg rosuvastatin or 80 mg simvastatin.

<h3>Key efficacy results</h3>
In adults with HeFH, Praluent75/150 mg 2QW led to significantly greater reductions in LDL-C compared to placebo (Figure 2), allowed a significantly greater proportion of patients to achieve a pre-specified LDL-C target compared to placebo (Figure 3) and LDL-C reductions were consistent and sustained over 78 weeks (Figure 4):
<ul>
 <li>At Week 24, mean percentage change in LDL-C was -48.8% (1.9mmol/L) (FH I) and -48.7% (1.74mmol/L) (FH II) for Praluent versus 9.1% (0.29mmol/L) (FH I) and 2.8% (0.07mmol/L) (FH II) for placebo (p&lt;0.0001 for both studies) (Figure 2)</li>
 <li>At Week 24, regardless of prior CV status, 59.8% (FH I) and 68.2% (FH II) of Praluent patients achieved pre-specified LDL-C target of &lt;1.8 mmol/L versus 0.8% (FH I) and 1.2% (FH II) of placebo patients (p&lt;0.0001 for both studies) (Figure 3)</li>
 <li>At Week 78, the mean reduction in LDL-C level with Praluent compared with placebo was -51.8% (1.9mmol/L) (FH I)&nbsp; and -52.1% (1.76 mmol/L) (FH II) (Figure 4).</li>
</ul>
Amongst Praluent patients who received double-blind treatment for at least 12 weeks, 56.6% (FH I) and 61.4% (FH II) had LDL-C levels &lt;1.8 mmol/L at Week 8 and therefore remained on Praluent 75 mg Q2W for the duration of the study. LDL-C responses were durable and were maintained (up to 78 weeks) in Praluent treated patients.

Figure 2: ODYSSEY FH I and FH II: Mean reduction in LDL-C from baseline to Week 52&nbsp;- Adapted from Kastelein JJP, et al. Eur Heart J 2015; 36:2996–30031

Placebo + MTD statin therapy ± other LLT 
 Praluent + MTD statin therapy ± other LLT *Praluent dose was 75 mg administered SC every two weeks, but if LDL-C level was ≥1.8 mmol/L at Week 8, a pre-specified dose up-titration to 150 mg every two weeks was performed at Week 12 †This number refers to the number of patients receiving Praluent (ITT analysis)1 
 ‡This number refers to the number of patients receiving placebo (ITT analysis)1

Figure 3: ODYSSEY FH I and FH II: Proportion of patients achieving LDL-C target at Week 24&nbsp;- (Adapted from Kastelein JJP, et al. Eur Heart J 2015; 36:2996–30031)

Placebo + MTD statin therapy ± other LLT 
 Praluent + MTD statin therapy ± other LLT *Praluent dose was 75 mg administered SC every two weeks, but if LDL-C level was ≥1.8 mmol/L at Week 8, a pre-specified dose up-titration to 150 mg every two weeks was performed at Week 12 †This number refers to the number of patients receiving Praluent (ITT analysis)1 
 ‡Intention to treat (ITT) analysis 
 &nbsp;

Figure 4: ODYSSEY FH I and FH II: Mean reduction in LDL-C from baseline to Week 781,2&nbsp;- (Adapted from Kastelein JJP, et al. Eur Heart J 2015;36:2996-3003)

Placebo + MTD statin therapy ± other LLT 
 Praluent + MTD statin therapy ± other LLT ‡Intention to treat (ITT) analysis
 
 *Praluent dose was 75 mg administered SC every two weeks, but if LDL-C level was ≥ 1.8 mmol/L at Week 8, a pre-specified dose up-titration to 150 mg every two weeks was performed at Week 121 
 †Statin therapy at the maximum-tolerated dose (40-80 mg atorvastatin, 20-40 mg rosuvastatin daily or 80 mg simvastatin [if on this dose for &gt;1 year]) or a lower dose, provided a reason was documented

<h2>Key safety results</h2>
Frequency of TEAEs and SAEs were similar in Praluent and placebo patients (Table 2). Although a higher proportion of Praluent than placebo patients experienced injection site reactions, these differences were non-significant (FH I, p=0.77; FH II, p=0.38); most reactions were mild and none lead to discontinuation (Table 2).

Table 2: ODYSSEY FH I and FH II: Treatment-emergent adverse events (safety population)&nbsp;- Adapted from Kastelein JJP, et al. Eur Heart J 2015; 36:2996–30031

<table cellpadding="20" style="width:100%;">
 <tbody>
 <tr>
 <td colspan="1" rowspan="2" style="background-color: rgb(0, 155, 195); width: 40%;">
 &nbsp;
 &nbsp;</td>
 <td style="background-color: rgb(0, 155, 195); width: 10%;">
 Praluent 
 75/150 mg 
 (n=322)</td>
 <td style="background-color: rgb(0, 155, 195); width: 10%;">
 Placebo 
 (n=163)</td>
 <td style="background-color: rgb(0, 155, 195); width: 10%;">
 Praluent 
 75/150 mg 
 (n=167)</td>
 <td style="background-color: rgb(0, 155, 195); width: 10%;">Placebo 
 (n=81)</td>
 </tr>
 <tr>
 <td style="background-color:#009bc3">
 FH I</td>
 <td style="background-color:#009bc3">
 &nbsp;</td>
 <td style="background-color:#009bc3">
 FH II</td>
 <td style="background-color:#009bc3">
 &nbsp;</td>
 </tr>
 <tr>
 <td>
 TEAE, n (%)</td>
 <td>
 263 (81.7)</td>
 <td>
 129 (79.1)</td>
 <td>
 125 (74.9)</td>
 <td>
 66 (81.5)</td>
 </tr>
 <tr>
 <td>
 Treatment-emergent SAEs, n (%)</td>
 <td>
 44 (13.7)</td>
 <td>
 22 (13.5)</td>
 <td>
 15 (9.0)</td>
 <td>
 8 (9.9)</td>
 </tr>
 <tr>
 <td>
 TEAE leading to discontinuation, n (%)</td>
 <td>
 11 (3.4)</td>
 <td>
 10 (6.1)</td>
 <td>
 6 (3.6)</td>
 <td>
 1 (1.2)</td>
 </tr>
 <tr>
 <td>
 Injection site reactions, n (%)</td>
 <td>
 40 (12.4)</td>
 <td>
 18 (11.0)</td>
 <td>
 19 (11.4)</td>
 <td>
 6 (7.4)</td>
 </tr>
 <tr>
 <td>
 TEAEs leading to death, n (%)</td>
 <td>
 6 (1.9)</td>
 <td>
 0</td>
 <td>
 0</td>
 <td>
 0</td>
 </tr>
 <tr>
 <td colspan="5">
 Safety events of interest</td>
 </tr>
 <tr>
 <td>
 Positively adjudicated CV adverse events, n (%)</td>
 <td>
 8 (2.5)</td>
 <td>
 3 (1.8)</td>
 <td>
 2 (1.2)</td>
 <td>
 1 (1.2)</td>
 </tr>
 <tr>
 <td>
 General allergic TEAEs, n (%)</td>
 <td>
 28 (8.7)</td>
 <td>
 16 (9.8)</td>
 <td>
 19 (11.4)</td>
 <td>
 5 (6.2)</td>
 </tr>
 <tr>
 <td>
 Neurological TEAEs, n (%)</td>
 <td>
 12 (3.7)</td>
 <td>
 7 (4.3)</td>
 <td>
 7 (4.2)</td>
 <td>
 2 (2.5)</td>
 </tr>
 <tr>
 <td>
 Neurocognitive disorders, n (%)</td>
 <td>
 2 (0.6)</td>
 <td>
 2 (1.2)</td>
 <td>
 0</td>
 <td>
 1 (1.2)</td>
 </tr>
 <tr>
 <td>
 Development/ 
 worsening of diabetes, n (%)</td>
 <td>
 6 (1.9)</td>
 <td>
 4 (2.5)</td>
 <td>
 4 (2.4)</td>
 <td>
 2 (2.5)</td>
 </tr>
 <tr>
 <td>
 Ophthalmologic disorders, n (%)</td>
 <td>
 3 (0.9)</td>
 <td>
 4 (2.5)</td>
 <td>
 3 (1.8)</td>
 <td>
 1 (1.2)</td>
 </tr>
 <tr>
 <td>
 Alanine aminotransferase, &gt;3 x ULN (%)</td>
 <td>
 5/322 (1.6)</td>
 <td>
 2/163 (1.2)</td>
 <td>
 6/166 (3.6)</td>
 <td>
 1/81 (1.2)</td>
 </tr>
 <tr>
 <td>
 Creatine kinase, &gt;3 x ULN (%)</td>
 <td>
 13/318 (4.1)</td>
 <td>
 10/163 (6.1)</td>
 <td>
 8/165 (4.8)</td>
 <td>
 6/80 (7.5)</td>
 </tr>
 </tbody>
</table>

Please refer to publication for full safety profile information
CV = cardiovascular; SAEs, serious adverse events; TEAE = treatment-emergent adverse events

<h2>Conclusions</h2>
<ul>
 <li>Praluent 75/150 mg every 2 weeks significantly lowered calculated LDL-C from baseline to Week 24 in patients with HeFH on top of the maximum-tolerated dose of statin compared to placebo (-48.8% (1.9mmol/L) (FH I) and -48.7% (1.74mmol/L) (FH II) for Praluent versus 9.1% (0.29mmol/L) (FH I) and 2.8% (0.07mmol/L) (FH II) p &lt;0.0001 for both studies)</li>
 <li>At Week 24, 59.8% of patients in the FHI study and 68.2% in the FHII study achieved the pre-specified target LDL-C level of &lt;1.8 mmol/L compared to 0.8% (FHI) and 1.2% (FHII) patients on placebo (p&lt;0.0001 for both studies)</li>
 <li>At week 8, over 50% of patients achieved pre-specified LDL-C target of &lt;1.8 mmol/L and were maintained on the 75mg dose</li>
 <li>The incidences of TEAEs and treatment-emergent SAEs were similar between treatment groups over 78 weeks of treatment 
 &nbsp;</li>
</ul>
‡HeFH diagnosed by either genotyping or clinical criteria (Simon Broome or World Health Organization/Dutch Lipid clinic network score of &gt;8)
**Maximum-tolerated statin dose defined as 40–80 mg atorvastatin, 20–40 mg rosuvastatin or 80 mg simvastatin, or lower dose if documented reason provided e.g., intolerance or local practice
†Established CHD defined as acute myocardial infarction, silent myocardial infarction, unstable angina, coronary revascularisation, or clinically significant CHD diagnosed by invasive or non-invasive testing. CHD risk equivalents defined as ischaemic stroke, peripheral artery disease, moderate chronic kidney disease, or diabetes (only if ≥2 risk factors present)
§High-dose statin therapy defined as 40–80 mg atorvastatin, 20–40 mg rosuvastatin or 80 mg simvastatin

<a href="/uk/dyslipidaemia">SEE MORE FROM SCIENCE</a>

<h3>Praluent®</h3>
Find more information on Indication, Administration and Mechanism of Action and watch videos about Praluent®.

<h3>Patient Website</h3>
Find resources and support for your patients on Praluent®. Find useful links about how patients can manage their cholesterol.

<h2>Get in touch with the Dyslipidaemia Team</h2>

Praluent® (alirocumab) Prescribing Information (GB)

Praluent® (alirocumab) Prescribing Information (NI)

DYSLIPIDEMIA

CARDIOLOGY

FH I & FH II Studies Praluent® (alirocumab)

<h2>ESC/EAS 2019 guidelines recommend more aggressive treatment to reach LDL-C goals1</h2>
<h3>The LDL-C goal has been reduced to &lt;1.4mmol/L for patients at very high CV risk in the 2019 ESC/EAS guidelines</h3>

CV&nbsp;= cardiovascular;&nbsp;EAS&nbsp;= European Atherosclerosis Society;&nbsp;ESC&nbsp;= European Society of Cardiology;&nbsp;LDL-C&nbsp;= low-density lipoprotein cholesterol.

<h3>Results of the EUROASPIRE V survey - most coronary patients have a less than optimal management of LDL-C&nbsp;3*</h3>
<ul>
 <li>Only half of the patients (n = 3811) were on high-intensity LLT 
 (men = 51.3%; women = 46.0%)</li>
 <li>The high-intensity LLT related to 72% on atorvastatin 40–80 mg/d, 20% on rosuvastatin 
 20–40 mg/d and 8% were on combinations of statins with ezetimibe.</li>
</ul>

*The EUROASPIRE V survey used standardized methods were used by trained technicians to collect information on 7824 patients from 130 centres in 27 countries (including Ireland), from the medical records and at a visit at least 6 months after hospitalization for a coronary event (elective CABG, an elective PCI or an acute coronary syndrome).
CABG&nbsp;= coronary artery bypass graft;&nbsp;LDL-C&nbsp;= low-density lipoprotein cholesterol;&nbsp;LLT&nbsp;= lipid lowering therapy;&nbsp;PCI= percutaneous coronary intervention

<h2>ESC/EAS 2019 guidelines recommend more aggressive treatment to reach LDL-C goals1</h2>
<h3>51% of very high-CV-risk patients would not reach ESC/EAS 2019 Guideline LDL-C goals4</h3>

Distribution of LDL-C levels at 1 year*

*At 1-year post-event based on a modelled LDL-C level of 1.4 &nbsp;mmol/L or greater on high-intensity statins and ezetimibe. Patient group contains 2,521 patients hospitalised for an ACS event. The ELIPS study (NCT01075867), a prospective, multicentre, observational cohort study of consecutive ACS patients that aimed to assess the quality of care and adherence to recommended preventive treatments at four academic centres in Switzerland. The analysis included all ACS patients who were enrolled between 1 January 2009 and 31 December 2017, were alive and had available data on LDL-cholesterol values and lipid-lowering therapies 1 year after &nbsp;the index ACS event.

Get in touch with the Dyslipidaemia Team

Unmet Needs in Dyslipidaemia

Antonio Ochoa-Ferraro speaks about the importance of collaborating and the emerging role of AI in the management of rare diseases.

<h2>In conversation with Antonio Ochoa-Ferraro – 
 Collaborating to innovate in rare diseases.</h2>

Watch the full interview with Antonio as he gives his perspectives on working in rare diseases and the potential impact of the Rare Disease Framework on clinical practice.

Antonio Ochoa-Ferraro, Specialist Pharmacist in Inherited Metabolic Disease

Dr Alex Broomfield explore the challenges and opportunities faced by the rare disease community.

<h2>In conversation with Dr Alex Broomfield – Challenges and opportunities in the field of rare disease</h2>

Watch the full interview with Dr Alex Broomfield.

Challenges and opportunities in the field of rare disease

Dr Alex Broomfield, Consultant in Inherited Metabolic Diseases at GOSH

This is intended for HCPs practising in Great Britain (England, Scotland and Wales) only.
<a href="${link:{uuid:{b396cd3c-8152-48f5-ae78-06924624d39e},repository:{dam},path:{/Portal/UK/Prescribing-links/Supemtek-PI-GB-April-2023.pdf}}}">Supemtek®</a>▼<a href="${link:{uuid:{b396cd3c-8152-48f5-ae78-06924624d39e},repository:{dam},path:{/Portal/UK/Prescribing-links/Supemtek-PI-GB-April-2023.pdf}}}">(Quadrivalent recombinant Influenza Vaccine, prepared in cell-culture) Prescribing Information</a>

Recombinant technology eliminates the possibility of adaptation or mutation by replicating only the haemagglutinin (HA) antigen, directly from a genetic sequence. The resulting antigens are an exact genetic match to the target strain.2,3
In the production of <a href="${link:{uuid:{1b34dd78-c3db-424c-997c-a35cbbf1e482},repository:{products},path:{/UK/supemtek}}}">Supemtek</a>, the HA antigen DNA for each World Health Organization (WHO)-recommended influenza strain is combined with host cell DNA.1,3 Because only the DNA for each influenza antigen is used, there is no live virus replication during the recombinant process.3
<a href="${link:{uuid:{1b34dd78-c3db-424c-997c-a35cbbf1e482},repository:{products},path:{/UK/supemtek}}}">Supemtek</a><a href="https://d2b918c201921t.cloudfront.net/hcp-portal-uk/uk/products/vaccines/influenza/supemtek"> </a>contains 3x more HA antigen (45 μg versus 15 μg) per strain, compared with cell- and egg-based standard-dose quadrivalent influenza vaccines.2
Discover more about how <a href="${link:{uuid:{1b34dd78-c3db-424c-997c-a35cbbf1e482},repository:{products},path:{/UK/supemtek}}}">Supemtek</a>, our recombinant flu vaccine, is manufactured:&nbsp;

&nbsp;Learn more about the advancements in influenza vaccine manufacturing technology.

INFLUENZA

VACCINES

Recombinant Flu Vaccine


<h2>Recombinant technology generates HA antigens that are an exact genetic match to the target strains2,3</h2>

This eliminates the possibility of adaptation or mutation.2,3
According to evidence gathered over previous flu seasons, influenza vaccine effectiveness against A/H3N2 influenza viruses may have been lower than against other influenza strains. This may be due to egg adaptation, resulting in an antigenic mismatch between the vaccine strain and strains circulating during a particular influenza season.5–8

Abbreviations

Learn more about the advancements in influenza vaccine manufacturing technology.

Dr Karolina Stepien speaks about the potential of multi-stakeholder collaboration to improve patient care.

<h2>In conversation with Dr Karolina Stepien – Changes in clinical practice based on The Rare Disease Framework</h2>

Watch the full interview with Dr Karolina Stepien as she gives her perspective on how The Rare Disease Framework will help address some of the key challenges in rare diseases.

Exploring how the Rare Disease Framework may support the earlier diagnosis of rare diseases

 Dr Karolina Stepien, Consultant in Metabolic Medicine at Salford Royal Hospital


<a href="${link:{uuid:{8cd02cf2-bd72-495f-b720-698ef8d3f0da},repository:{dam},path:{/Portal/UK/Prescribing-links/Toujeo.pdf}}}" target="_blank">Prescribing Information Toujeo (insulin glargine 300 units/mL)</a>

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Sanofi is here to support you and your patients.

<h2>Sparta Summary</h2>
In this clinical summary you discover the real-world evidence of Toujeo in people with T1 diabetes living in UK. This was conducted in the SPARTA study - a descriptive, retrospective study.

Sparta Video

In the short video (2.35 min) you’ll learn about the results of the SPARTA study in T1 diabetes. This descriptive, retrospective study represents the real-world experience of using Toujeo®&nbsp;in 300 patients with T1DM in the UK.

<a href="/uk/type-1-diabetes">SEE MORE FROM SCIENCE</a>

<h3>Toujeo</h3>
Toujeo®&nbsp;is indicated as treatment of diabetes mellitus in adults,&nbsp;adolescents and children from the age of 6 years.&nbsp;

<h3>Patient Website</h3>
Find resources and support for your patients on Toujeo®. Help patients understand the basics of living and staying well with diabetes and how to have a positive start and experience with the medication prescribed to them.

Toujeo® (insulin glargine 300 units/mL) Prescribing Information 

TYPE-1-DIABETES

DIABETES

SPARTA study

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Development of ADCT involved literature review as well as interviews with patients and physicians, and was funded by Sanofi and Regeneron.

The ADCT gives a measure of how controlled your patient’s eczema is. Use these 6 concise questions to evaluate all dimensions of atopic dermatitis control.

Atopic dermatitis, a type of eczema, may be affecting your patient’s life in more ways than you know.

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MAT-XU-2300297 (v3.0) - Date of preparation: October 2023

MAT-XU-2305062 (v1.0) - Date of preparation: November 2023

MAT-XU-2300297 (v3.0) Date of Preparation: October 2023

MAT-XU-2305047 (v1.0) - Date of preparation: November 2023

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MAT-XU-2300297 (v6.0) - Date of Preparation: April 2024

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