diff --git a/src/contents/Human Practices/Further Engagement/Education.tsx b/src/contents/Human Practices/Further Engagement/Education.tsx
index 224860aaface5a8a1923e0b3b346f04546bf0b31..361f6cd7b840c8eb1e2f856127da3e9d27cae0dc 100644
--- a/src/contents/Human Practices/Further Engagement/Education.tsx	
+++ b/src/contents/Human Practices/Further Engagement/Education.tsx	
@@ -1,6 +1,6 @@
 import { ButtonOne } from "../../../components/Buttons";
 import {  H4 } from "../../../components/Headings";
-import {  H2 } from "../../../components/Headings";
+import {  H5 } from "../../../components/Headings";
 import { LoremMedium } from "../../../components/Loremipsum";
 
 
@@ -26,24 +26,24 @@ export function HPEducation(){
             </div>
             <div id="akademie" className="edu-cycletab" style={{display: "none"}}>
                 <H4 id="student-academy-heading" text="Student academy on the topic of synthetic biology"/>
-                <H2 id="Scüler*innen Akademie" text="Teaching the Next Generation of SynBio Pioneers The Center for Biotechnology (CeBiTec) at Bielefeld University organizes the annual CeBiTec Student Academy for “Biotechnology and Biomedicine.” Supported by the Osthushenrich Foundation and the Detmold district government, the academy offers students a unique opportunity to deepen their understanding of biology, genetics, and molecular biology through hands-on experiments and expert lectures. Key topics include nanopore sequencing, tumor diagnostics, and the evolution of SARS-CoV-2. The program is especially valuable for students transitioning from school to potential studies in the natural sciences."/>
+                <H5 id="Scüler*innen Akademie" text="Teaching the Next Generation of SynBio Pioneers The Center for Biotechnology (CeBiTec) at Bielefeld University organizes the annual CeBiTec Student Academy for “Biotechnology and Biomedicine.” Supported by the Osthushenrich Foundation and the Detmold district government, the academy offers students a unique opportunity to deepen their understanding of biology, genetics, and molecular biology through hands-on experiments and expert lectures. Key topics include nanopore sequencing, tumor diagnostics, and the evolution of SARS-CoV-2. The program is especially valuable for students transitioning from school to potential studies in the natural sciences."/>
                 <p> 
 Due to our collaboration with the Student Academy, we conducted the nanopore sequencing experiment and served as teachers, assisting in experiment preparation, execution, offering guidance, and answering questions. This role allowed us to teach the students about laboratory work, the critical aspects of conducting experiments, and essential safety considerations. The experiment involved isolating bacterial DNA, preparing samples for sequencing, and performing both sequencing and data analysis. 
 Since we presented our iGEM project PreCyse to them as well, the students were introduced to study-related projects like iGEM. They learned about the daily tasks, challenges, and responsibilities involved in iGEM through project discussions. Many students were captivated by the iGEM concept and expressed interest in participating during their future studies. They were particularly fascinated by the opportunity to develop real research projects, work independently in the lab, learn extensively about synthetic biology, and implement creative ideas while collaborating with an international team.</p>
                 </div>
                 <div id="teutoruft" className="edu-cycletab" style={{display: "none"}}>
                     <H4 id="teuroruft-heading" text="Educational city tour for young and old"/>
-                    <H2 id="Der Teuto ruft!" text="“Der Teuto ruft!” and why we participate"/>
+                    <H5 id="Der Teuto ruft!" text="“Der Teuto ruft!” and why we participate"/>
                     <p> </p>
                 </div>
                 
 "Der Teuto ruft!" is an outreach event located all over the city of Bielefeld where various local companies and institutions engage with the public to inform them about their work. Since we wanted to raise awareness for cystic fibrosis and present our approach to developing an optimized gene therapy to combat this disease, our participation in the "Der Teuto ruft!" event in Bielefeld was the perfect opportunity to do so. 
-<H2 id="What was our strategy?" text="What is our strategy?"/>
+<H5 id="What was our strategy?" text="What is our strategy?"/>
 <p>Our goal was to educate children about the challenges faced by CF patients, especially the ones with lung problems. The knowledge which we gained at the Science Communication Workshop as part of the BFH Meetup was the optimal basis to plan our outreach to the public. We engaged the children with activities like coloring lung images and conducting experiments to experience and understand lung related symptoms.  
 One such experiment involved creating a lung model from balloons and straws, demonstrating the difficulty patients have in breathing by having the children blow into the straws. Additionally, we set up a tank with a mixture of starch and water to simulate mucus and placed a ball on top. The children tried to blow the ball across the surface, illustrating how hard it is for air to move through mucus compared to water, where the ball moved much more easily. 
 The very little ones could paint coloring pages which we designed and printed for them. For the adults, we provided information about our project and discussed the implications and potential of gene therapy for cystic fibrosis. These conversations made it abundantly clear that degrees of knowledge on this topic widely vary throughout the public and we were happy to fill in the existing gaps in people's knowledge and exchange points of view on gene therapy.  
 Moreover, we connected with other institutions and participants at the event. We shared our booth at Bielefeld’s “Skulpturenpark” on the outside with btS, the life science student initiative from Bielefeld University [LINK], with whose members we had stimulating discussions as well. We were more than delighted when the city of Bielefeld featured us on their Instagram, highlighting our presence during "Der Teuto ruft!". This collaboration helped us reach a wider audience and raise awareness about our research efforts.</p>
-<H2 id="conclusion? " text="What is our conclusion"/>
+<H5 id="conclusion? " text="What is our conclusion"/>
 <p>Despite the changeable weather, we could educate many people of Bielefeld's community about cystic fibrosis, our therapeutic approach and gene therapy in general and had the opportunity to improve our science communication for the future as well so it was a successful event! </p>
                 <div className="row align-items-center">
                     <div className="col">
diff --git a/src/contents/safety.tsx b/src/contents/safety.tsx
index c6e5b423eb915eef3d9d2ade9d096d2b2a9986df..c63e87842f3e402194d4680e4cd4e6008e049964 100644
--- a/src/contents/safety.tsx
+++ b/src/contents/safety.tsx
@@ -41,7 +41,7 @@ export const Safety: React.FC = () =>{
             <strong>Reverse transcriptase:</strong> Reverse transcriptase plays a central role in prime editing by specifically inserting the correction as DNA at the inserted nick using an RNA template provided by pegRNA. The correction of the complementary DNA strand then takes place via the natural cell repair mechanisms.  This ensures an exact correction of the target sequence. We checked the reverse transcriptase to ensure it could perform precise genome editing without introducing unintended mutations. This was important to minimize the risk of off-target effects that could lead to unexpected or harmful consequences.
             </p>
             <p>
-            <strong>pegRNA (Prime Editing Guide RNA):</strong> The pegRNA is a multifunctional RNA molecule that fulfils two essential tasks. Firstly, it serves as a standard <strong>guide RNA (gRNA)</strong> that binds specifically to the target DNA and thus marks the site of editing. Secondly, it contains an RNA template that encodes the desired DNA modification. This enables the precise integration of the genetic modifications at the target site. We evaluated pegRNA for its ability to specifically target and modified the intended DNA sequence. Ensuring its specificity was crucial to avoid the potential disruption of other genes.
+            <strong>pegRNA (Prime Editing Guide RNA):</strong> The pegRNA is a multifunctional RNA molecule that fulfils two essential tasks. Firstly, it serves as a standard guide RNA (gRNA) that binds specifically to the target DNA and thus marks the site of editing. Secondly, it contains an RNA template that encodes the desired DNA modification. This enables the precise integration of the genetic modifications at the target site. We evaluated pegRNA for its ability to specifically target and modified the intended DNA sequence. Ensuring its specificity was crucial to avoid the potential disruption of other genes.
             </p>
             <p>
             <strong>Nickase Cas9, CasX, Fanzor (SpuFz1):</strong> These modified nucleases are designed to cut only one strand of DNA. This leads to controlled and precise editing of the genome, as cutting only one strand minimizes the risk of unwanted double-strand breaks. CasX and Fanzor offer smaller alternatives to Cas9, which is particularly advantageous for use in cells or organisms where space and efficiency requirements in terms of the transport system are an issue. Fanzor, being a newly introduced endonuclease, was particularly scrutinized in our project to ensure its safety and effectiveness in different cellular contexts. 
@@ -53,13 +53,13 @@ export const Safety: React.FC = () =>{
             For our  cloning experiments and the development of our prime editing complexes, we have amplified various plasmids in <i>E. coli</i> K-12 strains (DH5α,10-Beta) When working with microbial strains such as <i>E. coli</i> K-12 strains,  a it's important to consider potential risks associated with their use, even though they are generally regarded as safe in laboratory settings. All experiments were performed under strict S1 conditions, following all relevant safety protocols. Below you will find an overview of the <i>E. coli</i> K-12 strains for our cloning experiments, submitted by us as a checkin and the specific safety measures:
             </p>
             <p>
-            <i>E. coli K-12</i> strains (DH5α,10-Beta): Although these strains are non-pathogenic and have been modified to minimize the risk of spreading antibiotic resistance, there remains a low risk of horizontal gene transfer, where genetic material could be transferred to other microorganisms, potentially leading to the spread of resistance genes or other traits. If accidentally released into the environment, <i>E. coli</i> K-12 strains could potentially interact with native microbial communities. While they are typically outcompeted in natural environments, there's a remote possibility of ecological disruption, particularly in microenvironments where they could find a niche.While these strains are non-virulent, they still pose a minimal risk to humans, particularly immunocompromised individuals, through accidental ingestion or inhalation in a laboratory setting. 
+            <strong><i>E. coli K-12</i> strains (DH5α,10-Beta):</strong> Although these strains are non-pathogenic and have been modified to minimize the risk of spreading antibiotic resistance, there remains a low risk of horizontal gene transfer, where genetic material could be transferred to other microorganisms, potentially leading to the spread of resistance genes or other traits. If accidentally released into the environment, <i>E. coli</i> K-12 strains could potentially interact with native microbial communities. While they are typically outcompeted in natural environments, there's a remote possibility of ecological disruption, particularly in microenvironments where they could find a niche.While these strains are non-virulent, they still pose a minimal risk to humans, particularly immunocompromised individuals, through accidental ingestion or inhalation in a laboratory setting. 
             </p>
             <p>
             We submitted  the yeast strain <i>Pichia pastoris</i> (SMD1163) for the protein expression of Fanzor.
             </p>
             <p>
-            <i>Pichia pastoris</i> (SMD1163): <i>Pichia pastoris</i> (SMD1163) is a widely used yeast strain for the expression of recombinant proteins. It is characterized by a methanol-inducible expression system (AOX1 promoter) and high cell growth rates, which makes it ideal for industrial applications. The strain can be easily genetically manipulated and can perform post-translational modifications, which supports correct protein production.
+            <strong><i>Pichia pastoris</i> (SMD1163):</strong> <i>Pichia pastoris</i> (SMD1163) is a widely used yeast strain for the expression of recombinant proteins. It is characterized by a methanol-inducible expression system (AOX1 promoter) and high cell growth rates, which makes it ideal for industrial applications. The strain can be easily genetically manipulated and can perform post-translational modifications, which supports correct protein production.
             When working with <i>Pichia pastoris</i> (SMD1163), various safety-relevant aspects must be observed. Although the organism is considered non-pathogenic and biologically safe (S1), skin contact and aerosol formation should be avoided to minimize the risk of infection or allergic reactions. When using genetically modified strains, it is important to follow the relevant GMO guidelines to prevent uncontrolled release. In addition, handling chemicals such as methanol requires special precautions as they are toxic and highly flammable. The disposal of cell cultures and waste must also be carried out in accordance with biosafety regulations, especially in the case of genetically modified organisms. 
             </p>
             <H4 text="Checkin for Testing in cell lines "></H4>
@@ -72,7 +72,7 @@ export const Safety: React.FC = () =>{
             <strong>HEK293T-3HA-F508del-CFTR cell line:</strong> The HEK293T-3HA-F508del-CFTR cell line is a modified HEK293T cell line that carries the F508del mutation in the CFTR gene, which is responsible for the most common mutation in cystic fibrosis. This mutation leads to a defective CFTR protein that impairs the normal function of the chloride channel. The cell line is therefore ideal for studying the effects of this mutation and for evaluating potential therapies for cystic fibrosis. 
             </p>
             <p>
-            <strong>CFBE41o- cell line:</strong> The CFBE41o- cell line, derived from the bronchial epithelial cells of a cystic fibrosis patient, is homozygous for the ΔF508-CFTR mutation and was essential for our cystic fibrosis research. . A reduced CFTR expression level is present. The cell line carries the CFTR defect and can therefore represent a patient with CF. The cell line is used to test our mechanism. These cells were immortalized with a replication-defective plasmid that retains their physiological properties.
+            <strong>CFBE41o- cell line:</strong> The CFBE41o- cell line, derived from the bronchial epithelial cells of a cystic fibrosis patient, is homozygous for the ΔF508-CFTR mutation and was essential for our cystic fibrosis research. A reduced CFTR expression level is present. The cell line carries the CFTR defect and can therefore represent a patient with CF. The cell line is used to test our mechanism. These cells were immortalized with a replication-defective plasmid that retains their physiological properties.
             When working with the HEK293T and CFBE41o- cell lines, it’s important to consider the minimal risks associated with their use. While not harmful on their own, the genetic modifications in HEK293T cells require careful handling to prevent accidental release or exposure. These cells, engineered to overexpress CFTR, including the F508del mutation, necessitate strict safety measures like regular monitoring and proper waste disposal to comply with S1 laboratory standards. Similarly, CFBE41o- cells, due to their genetic modifications and disease relevance, require careful handling to avoid cross-contamination and ensure biosafety.
             </p>
             <p>
@@ -93,10 +93,39 @@ export const Safety: React.FC = () =>{
       </Section>
       <Section title="Biosafety" id="Biosafety">
         <Subesction title="Mechanism" id="Biosafety1">
-          <LoremMedium/>
+          <p>
+          The biosafety of our Prime Editing complex has been a top priority throughout the entire development process. We have therefore tried to optimise all parts that influence the biosecurity of our system as much as possible. To ensure maximum biosecurity, we have created and tested many designs, as well as extensively researched alternatives and/or additional elements that contribute to biosecurity.
+          </p>
+          <H4 title="PAM disrupt"></H4>
+          <p>
+          A key safety mechanism incorporated in our design of the Prime Editing complex is the disruption of the PAM sequence. For the nickase enzyme to function properly, it must bind directly to the DNA strand, a process that is facilitated by the presence of a specific sequence called the PAM (Protospacer Adjacent Motif). This critical interaction occurs through the recognition of the PAM sequence by the nickase itself. To achieve PAM disruption, the pegRNA (prime editing guide RNA) is specifically designed in a way so that the PAM sequence is situated within the reverse transcription template (RTT) of the pegRNA. By introducing a silent mutation within the RT template into the PAM sequence. Therefore the PAM sequence is effectively eliminated after the gene editing process is successfully completed [1]. As a result of that, the PAM sequence is no longer present on the DNA strand, preventing the nickase from binding again at the same location. This reduction in repeated or undesired binding of the nickase enhances the safety of our prime editing complex, minimizing the risk of unintended edits or off-target effects in subsequent steps. Ultimately, this feature contributes very much to the overall safety and reliability of the prime editing process.
+          </p>
+          <H4 title="pegRNA design - Spacer"></H4>
+          <p>
+          Biosafety is also guaranteed by the careful selection of the spacer, which plays a critical role in guiding the complex to its intended target site [2]. To ensure both precision and safety, we meticulously chose and rigorously checked the spacer using the CRISPick software [3]. This allowed us to evaluate whether our Spacer would be likely to target other regions than our target site and therefore allowing us to analyse and predict potential off-target effects, ensuring that erroneous edits are minimised. By optimising the spacer selection, we have not only significantly enhanced the overall editing efficiency, striking a balance between precision and performance, but especially ensured the utmost accuracy in directing the Prime Editor, further contributing to the safety of the editing process. [Bild 1]
+          </p>
+          <H4 title="Riboswitch"></H4>
+          <p>
+          Riboswitches are segments of an RNA strand that bind to small molecules, causing them to change their secondary structure by forming hairpin structures. This process regulates gene expression at the translation level by preventing ribosomes from binding at the RBS and translating the coding region on the RNA strand. 0For our project we also considered an ion-sensitive riboswitch, specifically dependent on sodium ions (Na⁺), as a regulatory mechanism. The secondary structure of this riboswitch prevents the binding of ribosomes to the ribosome binding site (RBS) under normal conditions, thus inhibiting the translation of the subsequent mRNA. When sodium ions bind to the riboswitch, a structural change occurs, exposing the RBS, which allows for the translation of the mRNA and the production of our fusion protein which is the main component of our prime editing system and therefore of enormous importance for it to work [4]. In the context of the CFTR mutation and its effects on the cell, the elevated Na⁺ levels play a crucial role. Due to the dysfunctional CFTR channel, which fails to properly function as a chloride channel, the ENaC channel (epithelial sodium channel) becomes upregulated. This upregulation results in an increased transport of sodium ions into the cell, leading to a higher intracellular sodium concentration. This elevated Na⁺ concentration creates a specific ionic environment that could potentially be utilized to regulate our Prime-Editing complex in a targeted manner. Given these specific ionic changes in the cell, we could have a disease-specific regulation of our Prime-Editing system based on the ionic situation typical of this condition. However, despite the initial promise of this approach, after further research, we concluded that the riboswitch, even considering the ion levels within epithelial cells, is overall too nonspecific and therefore too unreliable as a regulatory mechanism. Although the ion levels in CFTR cells are much lower, there are still low concentrations of sodium ions, which can lead to the riboswitch not being completely switched off.
+          [Bild 2]
+          As a further approach to developing alternative riboswitch variants, we considered the possibility of an RNA-regulated riboswitch targeting the defective mRNA sequence of the genetically defective CFTR gene. The basic idea behind this concept was that the riboswitch specifically binds to a region on the CFTR mRNA containing the F508Δ mutation. This binding should induce a structural change in the riboswitch on our prime editing complex’s mRNA that ultimately leads to exposure of the RBS to allow translation of the downstream sequence. This mechanism would be designed to react specifically to the defective CFTR mRNA and only cause a change in the secondary structure in the presence of the specific mutation. The riboswitch could thus ensure selective and disease-specific activation of our prime editing complex, which would be of particular interest in the context of genetic diseases such as cystic fibrosis. However, we did not pursue this approach any further. A major reason for this was the lack of sufficient literature providing a sound scientific basis for this specific application of a riboswitch. In
+          addition, our research steered us in a different direction, particularly with regard to the alternative mechanism involving the XBP1 intron to regulate the prime editing system. This alternative seemed more promising and was based on an established regulatory mechanism that is triggered by cellular stress and specifically responds to misfolding processes.
+          </p>
+          <H4 title="XBP1 Intron"></H4>
+          <p>After extensive research, we discovered a regulatory system in eukaryotic cells, the XBP1 mechanism. The activation of XBP1 is an important mechanism that occurs as part of the Unfolded Protein Response (UPR), a cellular stress response triggered by the accumulation of misfolded proteins in the endoplasmic reticulum (ER). The ER is a key cellular component responsible for protein folding and transport. When many misfolded proteins accumulate in the ER, a specific regulatory mechanism is activated to reduce the stress on the ER. XBP1 activation is controlled by a protein called IRE1α, which is embedded in the ER membrane. IRE1α acts as a sensor for protein misfolding stress in the ER. Once IRE1α detects misfolded proteins, it dimerizes and becomes activated through autophosphorylation. This activation switches on the endoribonuclease activity of IRE1α, which is a crucial step in the activation of XBP1. The mRNA for XBP1 is continuously transcribed in the nucleus and transported to the cytoplasm, where it contains an intron that is not normally spliced out. This intron contains a stop codon, preventing the translation of a functional XBP1 protein. However, when ER stress activates IRE1α, the endoribonuclease domain of IRE1α splices this intron out of the XBP1 mRNA. This is an unconventional splicing event, as it occurs in the cytoplasm rather than in the nucleus. Once the intron is removed, the spliced XBP1 mRNA can be translated into a functional XBP1 protein. This activated XBP1 acts as a transcription factor, turning on genes that increase the protein-folding capacity of the ER and promote the degradation of misfolded proteins. In this way, XBP1 helps the cell cope with ER stress and restore balance in the protein-folding process. Thus, this mechanism originally functions within the cell in the context of ER stress to maintain ER function when protein folding is disrupted. [5] [6] Our idea was therefore to integrate this intron into the mRNA encoding our prime-editing complex and thus use this mechanism to ensure that a functional prime editor is only synthesized when there is a high accumulation of misfolded proteins in the cell (similar to F508del). This would therefore represent an optimal safety aspect, as our fusion protein, which is essential for prime editing, cannot be fully synthesised as long as the genetic defect is not present in the cell. Accordingly, this provides the security that no healthy cells, as well as correctly edited cells, cannot be edited, which is an enormous contribution to biosafety. However, there was too much uncertainty about the extent to which other factors, such as misfolded proteins that are not associated with the CFTR protein, play a role in this mechanism. And since we could not and did not want to take the risk of such factors initiating the system, we decided against using it. To clarify this unknown correlation, we have considered a future experiment in which we want to switch this intron in front of a fluorescent marker and express it in cells with defective CFTR in order to confirm/investigate the dependence of intron splicing and the presence of CFTR F508del.</p>
         </Subesction>
-        <Subesction title="Delivery" id="Biosafety2">
-          <LoremMedium/>
+        <Subesction title="Safety aspects of our Airbuddy" id="Biosafety2">
+          <H4 title="SORT LNP and Cytotoxicity"></H4>
+          <p>
+          We have carefully considered the biosafety aspects of our delivery system, starting with the decision between Adeno-associated viruses (AAV) or lipid nanoparticles (LNPs) as delivery systems. Our comparison revealed that the biocompatibility and safety of LNPs are paramount for our approach. That is why we chose selective organ-targeting (SORT) lipid nanoparticles (LNPs) [1] in the context of targeted pulmonary mRNA delivery. One of our primary concerns with the LNP was the potential cytotoxicity of polyethylene glycol (PEG), a common stabilizing agent in LNP formulations. Aware of the immune responses PEG can trigger, potentially leading to cytotoxicity [2], we aimed at optimizing its concentration in our SORT LNPs to minimize such reactions while maintaining therapeutic efficacy. By the use of low molecular weight PEG, we addressed this problem. To test weather our approach succeeded, we conducted MTT and proliferation assays to ensure that our LNP posed no cytotoxicity risks.
+          </p>
+          <H4 title="Precision of our SORT LNP"></H4>
+          <p>
+          To further improve safety, we focused on reducing off-target effects. By incorporating specific SORT molecules, such as permanently cationic lipids like DOTAP, we ensured that the nanoparticles are systematically directed to the lungs. This precise targeting is particularly beneficial for respiratory diseases, as it enhances therapeutic effectiveness while limiting the impact on non-target organs. Our outlook of antibody conjugation as surface modification of our LNP for cell type-specific delivery, more exactly club cells [3] and ionocytes [4] as CFTR-expressing lung epithelial cells, would round off this aspect.
+          </p>
+          <p>
+          In summary, our design strategy emphasizes both safety and efficacy. The careful optimization of components like PEG 2000 and the use of targeted delivery molecules allow SORT LNPs to deliver therapeutic agents directly to the lungs, reducing systemic exposure and minimizing side effects. This targeted approach ensures more effective treatments, especially for conditions requiring localized intervention.
+          </p>
         </Subesction>
       </Section>
       <Section title="Biosecurity" id="Biosecurity">
diff --git a/src/data/drug-data.tsx b/src/data/drug-data.tsx
index 15dd52a4eb4ca9da7f5771d8e20d87986dd03429..655e699e3a10e1882a9a52471cb40d421eb3e174 100644
--- a/src/data/drug-data.tsx
+++ b/src/data/drug-data.tsx
@@ -38,7 +38,7 @@ export const drugdata: (Array<DrugDatensatz>)  = [
                 text: ["Active ingredient(s): Combination of elexacaftor/tezacaftor/ivacaftor \n Indications: For CF patients aged 2 years and older with at least one F508del mutation à 85 % of CF patients \n Mechanism: Elexacaftor and tezacaftor act as correctors on misfolded CFTR and permit delivery to the cell surface, thereby improving the channel density at the plasma membrane, while ivacaftor as a potentiator acts on CFTR channels that have reached the cell surface and increase the gating and conductance of ions [5]. \n Administration: Oral tablets \n Approval: Approved by the EMA in 2020 "] },
             {
                 title: "Symdeko",
-                text: ["Active ingredient(s): Combination of tezacaftor and ivacaftor \n Indications: For CF patients aged 6 years and older with specific mutations in combination with F508del or with two copies of F508del mutation \n Mechanism: Tezacaftor acts as a corrector on misfolded CFTR and permit delivery to the cell surface, thereby improving the channel density at the plasma membrane, while ivacaftor as a potentiator acts on CFTR channels that have reached the cell surface and increase the gating and conductance of ions [5] \n Administration: Oral tablets \n Approval: Approved by the EMA in 2018"]
+                text: ["Active ingredient(s): Combination of tezacaftor and ivacaftor", "Indications: For CF patients aged 6 years and older with specific mutations in combination with F508del or with two copies of F508del mutation", "Mechanism: Tezacaftor acts as a corrector on misfolded CFTR and permit delivery to the cell surface, thereby improving the channel density at the plasma membrane, while ivacaftor as a potentiator acts on CFTR channels that have reached the cell surface and increase the gating and conductance of ions [5]", "Administration: Oral tablets", "Approval: Approved by the EMA in 2018"]
             },
         ]
     },