title: Proletarian Unity Party (Italy)

abstract: The Proletarian Unity Party was a far-left political party in Italy.

text:
# Proletarian Unity Party (Italy)

The **Proletarian Unity Party** (Italian: *Partito di Unità Proletaria*, **PdUP**) was a far-left political party in Italy.

## Origins

The PdUP was founded in November 1972 by the minority factions of two parties: the New PSIUP, led by Vittorio Foa and Silvano Miniati, which gathered those militants from the Italian Socialist Party of Proletarian Unity (PSIUP) who had not agreed on the decision to join the Italian Communist Party (PCI); and Socialist Alternative, led by Giovanni Russo Spena and philosopher Domenico Jervolino, which was composed of several renegades from the left wing of the Workers' Political Movement (MPL) who had opposed that party's earlier merger with the Italian Socialist Party (PSI). The new party's symbol was the hammer and sickle over the world, which it had inherited from the PSIUP.

In 1974 these members were joined by *Il Manifesto*, a group which had been expelled from the PCI some years earlier, and by the Autonomist Student Movement led by Mario Capanna. Together, they merged to form the **Proletarian Unity Party for Communism** (Italian: *Partito di Unità Proletaria per il Comunismo*). The now expanded party's founding congress was held on January 29, 1976. The leaders of the party's three main currents were: Miniati, Foa and Capanna (predominantly ex-PSIUP and far left-oriented, with a grounding in *operaismo* or "workerism"); Rossana Rossanda and Lucio Magri (who both hailed from *Il Manifesto*, and leant towards collaborating with the PCI and the communist-backed CGIL trade union); and Luigi Pintor (who headed a minor 'third force' that frequently maintained the balance of power). Magri was elected as the party's first national secretary.

During the 1976 general elections, the PdUP ran as part of an electoral coalition under the Proletarian Democracy (*Democrazia proletaria*; DP) banner. The party gained three seats in the Italian Chamber of Deputies (won by Magri, Eliseo Milani and Luciana Castellina) out of the coalition's total of six.

## Splits and alliances

By 1977, tension had begun to develop within the party between its ex-PSIUP/MPL founders and Magri's *Il Manifesto* faction. The latter was deeply disappointed by the failure of the Italian left to establish a national government, but its focus on capturing power at the very top had always gone against the grain of the party's *operaista* (workerist) roots, which were typified by Foa's public insistence that "the real issue \[for the party\] was workers' control: left-wing power must be rooted in the struggles of the factories." Consequently, on February 20, 1977, the two tendencies split to form separate sections, with the far-left *operaista* element under Foa and Capanna soon abandoning the PdUP altogether in order to help constitute Proletarian Democracy formally as a new party. Magri's majority had earlier absorbed the *Avanguardia Operaia* movement, but it too was to leave the PdUP in 1978 following the congress held at Viareggio that year. However, during its third congress in Rome in 1981, the party was joined by the Workers' Movement for Socialism (*Movimento Lavoratori per il Socialismo*; MLS), a Maoist group led by Luca Cafiero.

## Absorption into the PCI and later events

After the elections of 1983, the PdUP joined the PCI list, to which it had become closer after the PCI secretary Enrico Berlinguer had abandoned the *Historic Compromise* (a project for a PCI-Christian Democracy alliance).

On November 25, 1984, the PdUP merged into the PCI. When, in 1991, Achille Occhetto started the process of transforming the PCI into the social democratic-oriented Democratic Party of the Left (PDS), some former PdUP members declared their opposition to the move and joined the Communist Refoundation Party (PRC). After the latter withdrew from the centre-left Lamberto Dini government in 1995, many former PdUP members left the party to create the Movement of Unitarian Communists, which later was absorbed into the PDS' heir, the Democrats of the Left.

## Notable members

## Election results

### Italian Parliament

| Chamber of Deputies | | | | | | |
| --- | --- | --- | --- | --- | --- | --- |
| Election | Votes | % | Seats | +/– | Leader | Government |
| 1976 | into DP |  | 5 / 630 |  | Lucio Magri | Opposition |
| 1979 | 502,247 (9th) | 1.4 | 6 / 630 | 1 | Luciana Castellina | Opposition |
| 1983 | into PCI |  | 1 / 630 | 5 | Lucio Magri | Opposition |

### European Parliament

| European Parliament | | | | | |
| --- | --- | --- | --- | --- | --- |
| Election year | Votes | % | Seats | +/− | Leader |
| 1979 | 406,656 (9th) | 1.2 | 1 / 81 |  | Luciana Castellina |
| 1984 | into PCI |  | 0 / 81 | 1 | Lucio Magri |

### Regional elections

| Regions of Italy | | | | | |
| --- | --- | --- | --- | --- | --- |
| Election year | Votes | % | Seats | +/− | Leader |
| 1975 | 147,030 (9th) | 0.5 | 4 / 720 |  | Lucio Magri |
| 1980 | 372,102 (8th) | 1.2 | 8 / 720 | 4 | Luciana Castellina |

## InfoBox

| Proletarian Unity Party Partito di Unità Proletaria | |
| --- | --- |
|
| Abbreviation | PdUP |
| Founded | 1972 |
| Dissolved | 1984 |
| Merger of | New PSIUP
Socialist Alternative |
| Merged into | Italian Communist Party |
| Newspaper | *Unità Proletaria*
*Il manifesto* |
| Ideology | Communism
Socialism
Maoism |
| Political position | Far-left |
| European Parliament group | Technical Group of Independents (1979–84) |
| Colours | Red |
|  | |


title: Who Killed Archie?

abstract: "Who Killed Archie?" is a storyline from the BBC soap opera EastEnders. It began on 25 December 2009, Christmas Day, when the character Archie Mitchell, played by Larry Lamb, was murdered by an unseen person. Events leading up to and following the murder put several characters in the frame, in the style of a Whodunit mystery. The culprit was kept a tight secret within the production crew as well, with only seven people knowing the identity of the killer. The murderer was revealed as Stacey Slater during a live episode titled "EastEnders Live", broadcast on 19 February 2010, the show's 25th anniversary. Turner was told thirty minutes before the broadcast that Stacey was the killer, and actors rehearsed several possible endings. Finally, a two-hander episode between Stacey and her ex-lover Max Branning on 26 March 2010 explained how she killed Archie - who had previously been the show's main antagonist prior to the character's death and murder storyline.

text:
# Who Killed Archie?

"**Who Killed Archie?**" is a storyline from the BBC soap opera *EastEnders*. It began on 25 December 2009, Christmas Day, when the character Archie Mitchell, played by Larry Lamb, was murdered by an unseen person. Events leading up to and following the murder put several characters in the frame, in the style of a Whodunit mystery. The culprit was kept a tight secret within the production crew as well, with only seven people knowing the identity of the killer. The murderer was revealed as Stacey Slater (Lacey Turner) during a live episode titled "EastEnders Live", broadcast on 19 February 2010, the show's 25th anniversary. Turner was told thirty minutes before the broadcast that Stacey was the killer, and actors rehearsed several possible endings. Finally, a two-hander episode between Stacey and her ex-lover Max Branning (Jake Wood) on 26 March 2010 explained how she killed Archie - who had previously been the show's main antagonist prior to the character's death and murder storyline.

## Storyline creation and development

The storyline was created in spring 2009 during a story conference, where executive producer Diederick Santer, storyliner Dominic Treadwell-Collins, series consultant and lead writer Simon Ashdown, series producer Lorraine Newman, script producer Sharon Batten, and Controller of BBC Drama Production John Yorke were considering what to do for the Christmas Day 2009 and 25th anniversary episodes. They discussed the character Archie Mitchell and how everyone hated him, and decided on a storyline with characters' hatred and anger towards Archie building up before Christmas, with a peak on Christmas Day when he is killed and another for the reveal on the 19 February 2010 anniversary. They decided to keep the killer's identity a secret within the small group and decided to reveal it during a live episode so that the secret could be kept for as long as possible, and managed the story on a need-to-know basis. The live episode's director, Clive Arnold, became the seventh person to discover the identity of the murderer. They went through the characters to decide who would create a "shiver" moment, and decided against Janine, even though she could have done it, because she has killed before. The killer was going to be Archie's wife Peggy Mitchell (Barbara Windsor), until producers discovered Windsor had planned to leave the show, so they decided on Stacey. Although scripts initially diverted attention away from Stacey, Santer realised that drawing attention away from her too much might make it more apparent.

Santer said there were three big clues to the killer's identity, "one in the Christmas Day episode, one more recently than Christmas and there's another one that, if I were to tell you where it was, would perhaps give it away too easily," however, in a chat with Sharon Marshall shown on *This Morning* on 18 February 2010, he said the second clue was about halfway through the investigation and the third was "on screen but not necessarily in the programme". He also said that the outcome would be "surprising", "satisfying" and "in retrospect, inevitable", adding that "it makes sense". Santer confirmed the clues in an interview on the *EastEnders* website: on Christmas Day Stacey disappears and it is never explained why, and then reappears on Boxing Day appearing "not quite with it"; Stacey is the only character still sufficiently angry enough to spit on Archie's grave at his funeral; and Stacey is the first character to feature in the Christmas Day trailers.

Plans to broadcast the first ever live episode of *EastEnders* were announced by the BBC on 15 September 2009. Santer initially refrained from discussing the episode's plot, but commented that it would resolve a "big storyline" which would "keep the audience (as well as the cast and crew) guessing until the very last moment." Santer confirmed that Archie's killer would be revealed in the live episode, and that their identity would be kept secret until the night of broadcast, even from the cast member playing them. The *EastEnders* cast and crew had two weeks to rehearse the episode prior to its live transmission. The script was issued on the afternoon of 5 February 2010, written by Simon Ashdown. The first read-through took place on 8 February 2010, though producers held back the part of the script revealing Archie's true killer. Ten different possible endings were scripted and rehearsed, each showing one character confessing to the murder. The ten characters were Janine Butcher (Charlie Brooks), Jack Branning (Scott Maslen), Ronnie Mitchell (Samantha Womack), Max Branning (Jake Wood), Ian Beale (Adam Woodyatt), Phil Mitchell (Steve McFadden), Billy Mitchell (Perry Fenwick), Ryan Malloy (Neil McDermott), Peggy and Stacey. Santer reiterated that the actor playing the killer would only be told so thirty minutes before the broadcast. He explained that the killer "may be revealed to the audience rather than the Square", preserving secrecy as the crew began filming episodes to be transmitted after the live broadcast. Brooks, who plays Archie's former lover Janine, found the secrecy difficult to work with, explaining: "In the episodes to be shown afterwards, you're being told to look or speak a certain way, but not why." Santer confirmed that the cast found the episode challenging, stating: "They are as desperate to know who did it as the viewers." Actor Charlie Clements, who played Bradley Branning, announced in November 2009 that he would be leaving the soap in 2010.

The moment Turner was told Stacey was the killer was filmed for a live reaction show broadcast immediately after "EastEnders Live" on BBC Three, though it was not broadcast. *EastEnders Live: The Aftermath* was presented by Lamb's son George and included other behind-the-scenes material. Turner received a call to see Santer about 20 minutes before the broadcast, where she was told that Stacey was the killer. She explained that she had no idea her character was the murderer, even after receiving the call. She hoped viewers would sympathise with the character as she not only has to deal with the guilt of killing Archie but was also inadvertently responsible for Bradley's death. Wood was also told as he supported Turner in the final scene in which she was revealed as the killer. Santer also brought in Maslen and McDermott as decoys in case other cast and crew members realised. Following the live episode, a two-hander episode featuring Max and Stacey was announced. The episode, broadcast on 26 March 2010, explains how and why Stacey killed Archie.

### Later development

Although the true identity of Archie's killer is kept a secret between Max and Stacey for several months, Max's daughter Lauren Branning (Jacqueline Jossa) becomes suspicious in November 2010 when Max tells her Bradley was innocent. Lauren suspects Max killed Archie as she becomes paranoid about his anger. Jossa said in an interview with website Digital Spy: "\[Lauren\]'s thinking about Archie's murder and realising that if Bradley didn't do it, it must have been someone else. As far as she knows, her dad is the only person who knows that Bradley didn't do it, so she's trying to put this puzzle together and it's all adding up to Max being the killer, because everything he does seems to lead to a lot of aggression." However, Lauren soon works out that Stacey is the murderer after speaking to her. Jossa said she was excited that her character was one of only a select few to know the true identity of Archie's killer.

## Suspects and motives

There were officially ten suspects for the murder, though the ten were not known to viewers or cast members, who speculated about the identity of the killer. On Christmas Eve, storylines showed Archie evicting his wife Peggy, daughters Ronnie and Roxy, Peggy's son Phil and Phil's son Ben (Charlie Jones) from their home, The Queen Victoria public house, after he became the landlord. Ronnie had a further motive as Archie had caused her to suffer a miscarriage and she blamed him for the death of her daughter Danielle Jones (Lauren Crace) earlier in 2009. Peggy discovered that Archie had paid her daughter Sam Mitchell (Danniella Westbrook) to skip bail, thus plunging the Mitchells into debt, and Sam returned on Christmas Day to discover she had been manipulated. Phil was also a suspect after failing to kill Archie on Peggy's request earlier in 2009. Simons explained that the killer was likely to be the most unsuspecting person, and stated that Roxy was "pretty much the only non-suspect," but said she felt the character would not go so far as to kill her father, even though she had seen his true colours. Woodyatt said his character, Ian Beale, would have done anything to stop his wife Jane (Laurie Brett) from finding out that he had sex with Janine, so it would be plausible if it turned out that Ian had killed Archie. Archie had a laptop recording of Ian and Janine together that he had threatened to give to Jane. Janine, who was engaged to Archie, also had a motive as Archie had been using her to gain ownership of The Queen Victoria and threw her out on Christmas Day. She was seen holding a knife before Archie was killed.

McDermott said his character, Ryan Malloy, "probably would have the balls to kill Archie" and it would be a possibility due to the character's past, although he accused Janine of the murder, making it unlikely unless he was "quite conniving." He stated Ryan's only motive would be out of love for Janine. Glynis Barber, who plays Archie's first wife Glenda Mitchell and was not seen in the programme until after the murder, said her instinct was that Glenda did not kill Archie, even though she had been told it was possible. Bradley Branning's motive came from the discovery that Archie raped his partner Stacey, and Clements said that if other characters knew, it would give Bradley a motive and the fact that Bradley punched Archie would make him a prime suspect. He stated that he hoped Bradley was not the killer, though in an interview with daytime television show *This Morning*, he stated it would be "quite historical to go down as the one who killed Archie Mitchell". The rape also gave Stacey a motive, and before she was sectioned in 2009 for bipolar disorder she accused Archie of trying to kill her. Jack Branning's motive came from his love for Ronnie and hatred of Archie, and he threatened Archie on Christmas Day. Maslen said it would be "great" if Jack was the murderer, but added that he may have taken the blame if Ronnie was guilty. Other possible suspects included Peggy's son Grant Mitchell (Ross Kemp), Billy Mitchell and Tracey the barmaid (Jane Slaughter). Slaughter said Tracey's only motive would be to protect The Queen Victoria or one of the Mitchells.

Odds on the killer's identity changed frequently in the fortnight preceding the transmission of "EastEnders Live". On 5 February, the clear favourite was Stacey Slater, with odds at Bodog of 2/1. By 9 February, Stacey's odds had shortened to 6/4, though the character dropped into third place by 12 February, usurped by her brother Sean Slater (Robert Kazinsky), who was last seen in the soap on 1 January 2009, at odds of 9/4, and Ben Mitchell at 7/2. On 14 February, the unlikely favourite became Tracey the barmaid, a background character whose odds shortened considerably from 40/1 to 11/4. Sean moved back into first place on 16 February, with odds of 2/1, and remained there until the eve of broadcast. Stacey Slater's odds fell to 16/1. William Hill had Sean as the favourite on 18 February with odds of 4/7, though on the morning of 19 February, Ben became the bookmakers' favourite. Polls on both the BBC website and on Digital Spy that ran in the week leading up to the live episode showed Bradley Branning as the person viewers most expected to be the killer, followed by Jack Branning, Ben Mitchell, Sean Slater and Sam Mitchell.

## Plot

### Events leading up to the murder

On Archie Mitchell (Larry Lamb) and Peggy Mitchell's (Barbara Windsor) wedding day, the true identity of Danielle Jones (Lauren Crace) as Ronnie Mitchell's (Samantha Womack) daughter is revealed. Archie has told Ronnie that her daughter, whom he gave up for adoption as a baby, has died. Just after Ronnie realises the truth, Danielle is hit by a car driven by Janine Butcher (Charlie Brooks) and dies in Ronnie's arms.

Peggy throws Archie out and asks her son Phil Mitchell (Steve McFadden) to kill him, but Phil just forces him to leave. The Mitchells also form a new rivalry with Janine, as she was the one responsible for hitting Danielle with her car and causing her death.

Ronnie is the most hurt about this and struggles to cope. She starts another relationship with Jack Branning (Scott Maslen), leading to their engagement. However, upon realising she wants another baby, she leaves Walford for a while, selling her portion of the club to Jack, who in turn gives it to Archie. After returning, Ronnie sleeps with Ryan Malloy (Neil McDermott) and Owen Turner (Lee Ross), and becomes pregnant with Owen's child.

Stacey Slater (Lacey Turner), Danielle's best friend in Walford, is also deeply affected by the incident, which triggers her bipolar disorder. She becomes non-compliant with her medication, has sex with Ryan, and is raped and attacked by Archie at the launderette. She believes both men are planning to kill her and is involuntarily committed to hospital, where she befriends Becca Swanson (Simone James). Upon her return to Walford along with Becca, Stacey restarts a relationship with Bradley Branning (Charlie Clements) when he rejects his girlfriend Syd Chambers (Nina Toussaint-White) for her.

When Archie returns, he attempts to reconcile with Peggy, but comes up with a plan to steal the Mitchells' business, The Queen Victoria public house, with Janine's help. However, Janine, along with Ryan, whom she is dating, plans to steal it from Archie at the last minute. Peggy's daughter Sam Mitchell (Danniella Westbrook), who has been in Brazil on the run from police due to her involvement in the murder of Den Watts (Leslie Grantham), returns to Walford, thinking the charges have been dropped. She is subsequently arrested, and the Mitchells put up £250,000 bail to have her released. Archie convinces Sam to leave again, paying for her to go. Phil is then forced to take out a loan from Ian Beale (Adam Woodyatt). Ian accepts, on the condition that if the loan is not paid back within a certain time, he becomes owner of The Queen Victoria. Archie and Janine learn of this and try to get Ian to sell the loan to them. When Ian's wife Jane Beale (Laurie Brett) leaves him, Janine gets him drunk and has sex with him, making an audio recording of them together. Archie and Janine blackmail Ian into selling them the loan and Archie tells the Mitchells they are trespassing. Once Archie finds out that Janine plans to fleece him, he proposes to her to keep her from going astray. Ryan is hurt by this setback and ends his relationship with her. Ronnie stands up to Archie and he pushes her into the bar, not knowing she is pregnant, though Roxy Mitchell (Rita Simons) then reveals it. Ronnie has a miscarriage and Peggy tells Archie he has killed another of Ronnie's children, warning him to stay away from her. Peggy eventually hands over the keys and the family of Peggy, Phil, Ronnie, Roxy, Ben Mitchell (Charlie Jones) and Roxy's baby Amy Mitchell leave on 24 December 2009. They end up being taken in by Jack, who vows revenge on Archie.

On Christmas Day, Archie tells Ian the CD of the recording is under Ian's Christmas tree for Jane, but Ian fails to find it. Archie tells Janine that they should skip Christmas dinner as he has made a surprise treasure hunt for her. Janine eventually finds an envelope containing a one-way ticket to Gdańsk, Poland and Archie throws her out onto the street telling her he knows how she and Ryan tried to double-cross him. Archie is visited by Jack who threatens to kill him if he hurts Ronnie again. Archie finds Ian searching his living room for the CD and Archie says it is on his laptop and he can make copies at any time, threatening Ian with a phone call to Jane, before ejecting him from the pub. Ian leaves, though not before telling Archie that if he does call Jane he'll wish he was dead. Sam then returns and attempts to confront Archie but he shuts the door on her. Ronnie subsequently arrives and tells him with no emotion that he will not make her care for him and she would not care if he died. Archie, after explaining how his father never smiled at him once and the impact had practically taught him to do the same, throws her out onto the street reminding her that it was the exact spot she pushed Danielle onto the night she died.

Shortly afterwards, Archie is visited by Peggy and he pleads with her to come home to him as she is the woman he loves. Peggy says she is not just a sweet and innocent old lady and that he has no idea who he is messing with. She tells Archie if he does not leave the pub that night he will regret every cruel and evil act he has ever done. He tells her that unless she returns he will have the pub converted to flats. He then becomes emotional as he tells Peggy that he will be waiting for her as she walks out on him. Bradley walks in and punches Archie in the face twice but accidentally punches the bar as well, cutting his hand. He tells Archie to stay away from his girlfriend Stacey because she has said Archie raped her three months previously which resulted in her becoming pregnant with his child, and Bradley leaves. As Archie picks up his snowglobe from the floor, the bust of Queen Victoria is pushed from the bar and hits him on the head.

### After the murder

Ronnie finds Archie on the floor of The Queen Victoria and he apologises to her before he dies. When the police are notified of the death they arrest Ronnie, but later release her without charge. DCI Jill Marsden (Sophie Stanton) investigates the rest of the Mitchell family. Phil is given a false alibi by his friend Shirley Carter (Linda Henry), who finds a blood-stained shirt amongst his belongings. Phil explains that he found Archie dead and lost his balance, falling into the blood, but did not call the police because he panicked. They burn the shirt, and when Marsden visits them again, asking to see the clothes Phil was wearing at Christmas, Shirley produces a freshly laundered one. Shirley's flatmate Heather Trott (Cheryl Fergison) reveals that Phil was not really with Shirley on Christmas Day, prompting Shirley to make an anonymous call stating she saw Janine enter The Queen Victoria on the day of the murder, deflecting suspicion from Phil. Peggy and Phil attempt to pin the murder on Sam, who retaliates by blaming Peggy. Both are questioned by Marsden at the police station, and though Peggy is released without charge, Sam is arrested for breaking her bail.

Ian has Archie's laptop, and though he deletes the audio file of him and Janine from it, it later comes to light, and he and Jane throw the laptop into the canal. Janine attempts to blackmail Ian, and when he rebuffs her, she tells the police about the recording and the laptop, leading to his arrest. Ian admits to stealing the laptop from The Queen Victoria on Christmas Day, but denies murder. The police charge him with murder, but when Janine admits the truth, the charges are dropped.

Marsden and her colleague DC Wayne Hughes (Jamie Treacher) attend Archie's funeral, but do not see Stacey spit on Archie's grave. Jack, a former police officer, tells Hughes he can help out with any "local information" they might need. After the funeral, Bradley proposes to Stacey at the car lot, and she accepts. Jack later learns that Archie raped Stacey, that she is now pregnant with what she believes is Archie's baby, and that Bradley punched him on Christmas Day. Jack urges Bradley to tell the police what he did, desiring to keep Ronnie out of trouble. Marsden reveals she has a new forensic profile and a DNA screening process will begin. She asks all white males to volunteer for DNA screening, and when Bradley complies, Jack bribes Hughes to make the samples disappear.

A ring Roxy inherited from Archie, which went missing at Christmas, is planted in Janine's flat. Marsden receives an anonymous tip-off and Janine is arrested after the ring is found in her teapot. She is interviewed, but is released due to lack of evidence. She realises that Peggy planted the ring in an attempt to frame her. When Shirley thinks Phil is seeing another woman, she accuses him of only being interested in her for her alibi. He says it is not true, but she drunkenly threatens to withdraw the alibi, and walks to the police station.

Becca becomes hurt upon realising that Bradley and Stacey are getting married. While they are away at their own wedding, Becca steals a hairbrush with Archie's hair from The Queen Victoria, intending to have a DNA test done on Stacey's baby to prove if it is really Archie's. However, she has doubts and goes back with Stacey to return the brush, but is caught by Ronnie. Becca coerces Stacey to confess Archie raped her and the baby is his. However, Ronnie tells Stacey that Archie underwent an operation a few years back that left him infertile, meaning that Stacey's baby is not his. Roxy accuses Ronnie of murdering Archie. Ronnie denies it, but tells her she found out about Archie raping Stacey, and admits that Archie had also raped her as a child. Peggy tells the two of them that when Archie was murdered, she found him lying on the floor, took her divorce papers from the bar and left him to die. Phil tells Peggy about his alibi, the shirt and that he found Archie dead on Christmas Day. Shirley then returns and says Phil has got away with it as she has not told the police anything. Meanwhile, Becca anonymously reports to the police that Bradley had a motive for the murder.

Jack receives a call from Hughes to say that Bradley is about to be arrested and urges Bradley to leave Walford as quickly as possible. Bradley and Stacey quickly pack their bags at home. Max Branning (Jake Wood) says an emotional goodbye to his son and Jack agrees to help them escape. They leave via the back door as Max delays the police at the front, and hide a few streets away. Jack also leaves by the back door but Marsden sees him and he is unable to meet Bradley and Stacey, who are nervously waiting. Bradley says they should go without Jack, but when they go to get a taxi to St Pancras railway station, Bradley realises he has left the passports at home and goes back to get them, leaving Stacey to wait. However, Stacey grows impatient and phones him. The police notice him when his phone rings, and in a bid to escape them, he runs up a fire escape and crawls across the roof of The Queen Victoria with an officer following him. He shouts at Stacey to run, but stumbles and falls backwards from the roof to his death as the residents look on in horror. Max and Stacey are devastated, and he pulls her away from the body. She tells him it is her fault, as Bradley did not kill Archie, she did. The following day, Marsden says the police will no longer be pursuing the investigation. Stacey then goes missing, and on the day of Bradley's funeral, Jack receives news that a court has found Bradley guilty of Archie's murder.

Max tracks down Stacey to a flat where Stacey explains that she was angry at Archie and was worried about what Bradley would do to him after he found out about the baby. A minute after Bradley confronted Archie, she found Archie on the floor and, lucid and angered at what he had done to her and to Danielle, pushed the bust onto his head, but ran after his fingers twitched, fearing he would call the police. Stacey reveals that she did not initially tell Bradley the truth about what she did that night, fearing that he would take the blame for her. When she finally told him while they were packing on their wedding night, she offered to confess to the police herself, but he convinced her to flee Walford with him regardless. After forcibly trying to make her confess to the police, Max eventually tells Stacey that no one else needs to know that she killed Archie, reasoning that Bradley would want her to be happy, and sends her home. Becca continues to live with Stacey, and tries to exclude Stacey's mother Jean Slater (Gillian Wright) from her life. However, when Jean reveals Becca's involvement in Bradley's death, Stacey slaps Becca, which causes her to have a meltdown leading to getting kicked out by Jean as Stacey tells her mother she can trust her again. Later, Stacey figures out that Ryan must be her baby's father but decides not to tell him so as to not complicate his rekindled relationship with Janine, even when he is with her in the hospital as she gives birth to her daughter Lily. Several months later, at Janine and Ryan's wedding reception, Stacey confesses her fear about Archie still being alive to Peggy, who tells Stacey that Archie is dead and that Bradley killed him, accidentally causing Stacey to confess the truth to her. Peggy wants to call the police but after a fire at The Queen Victoria, Peggy tries to convince Stacey to admit to arson as the sentence would be a lot less than that for murder. She leaves Walford while letting Stacey take care of Lily who needs her. Stacey also tells Ryan that he is Lily's father, and although he initially refuses to acknowledge her, he later bonds with her and gets used to the idea of being a father while Janine and Stacey are arrested on a night out. Upset with this, Janine attempts to sabotage his relationship with Stacey, but her actions inadvertently cause them to realise their growing attraction to each other.

Max's daughter Lauren Branning (Jacqueline Jossa) becomes angry at Max for never mentioning Bradley, leading to his confessing that he knows Bradley did not kill Archie. Lauren starts to suspect Max as he has become violent towards other people, but he tells her he promised to look after the real killer, who is no longer a danger. When Lauren sees Stacey dancing with Max, she accuses her of flirting with Max, but Stacey says they are just friends and he promised he would always look out for her. Lauren realises that Stacey is the killer and tells Max she knows this. She confronts Stacey, who confesses, and Lauren records it on her mobile phone. Lauren later hands the recording to Janine as Stacey and Ryan have begun having an affair. Max wipes the recording so on Christmas Eve, Janine publicly announces in the pub after trying to play the recording that Stacey killed Archie. Outside, Stacey privately tells Ryan that Janine is telling the truth.

As Christmas Day runs through, Stacey experiences numerous upsetting thoughts about her role in Archie's death, and tells Jean about this. Upset, Jean takes Lily away from her, and things are made worse when Janine attempts to frame Stacey by stabbing herself while placing the knife in Stacey's hands and convincing Jean to call the police. Stacey considers suicide, but Max offers to help her flee the country. On the way, Stacey convinces Jean that Janine has framed her for the stabbing, and breaks off her romance with Ryan when he offers to come with her. Before Stacey and Max leave Walford with Lily, Ronnie and Roxy confront Stacey about the truth. Although Roxy wants her jailed, Ronnie quickly tells Stacey to go, feeling that she has suffered enough. Max drives Stacey to the airport, and tells her that he still loves her, offering to leave the country with her. Stacey tells him that the only man she has ever loved is Bradley. They share a teary and emotional goodbye with each other as Max watches Stacey leave for her flight. Stacey is last seen holding Lily in her arms while on the plane.

In 2014, Stacey is found living in London using a false name. Her cousin Kat Moon (Jessie Wallace) brings her back to Walford. Stacey is still wanted by the police for stabbing Janine, and is eventually seen by Ronnie and Roxy. Roxy threatens to call the police but Ronnie convinces her not to. However, after Janine drops the charges, Stacey decides that she needs to clear Bradley's name, so tells the police she killed Archie. She is subsequently sentenced to five years in prison, but she decides to appeal the sentence, taking her bipolar disorder into account. The appeal is successful and Stacey is released.

In 2019, while Stacey's old friend Ruby Allen (Louisa Lytton) tries to find some closure after being raped, she learns what Archie did to Stacey and they visit his grave together - with Ruby convincing Stacey to get the closure she needs in order to move forward with her life. Stacey does so by telling Archie off for his actions against her and ruining her life, before concludingly telling him he cannot hurt her anymore - nor does he deserve any sympathy from her or anybody else.

## Reception

Overnight figures showed that Archie's murder on 25 December 2009 was watched by 45.9% of the viewing audience for that time, an average of 10.9 million and a peak of 11.9 million. It was the most watched TV show on Christmas Day 2009 in the UK. The following episode where the murder was discovered was also the most watched show of the day, with overnight ratings of 8.1 million, representing a 37.9% audience share. The investigation storyline helped *EastEnders* become the most watched soap opera on British television for the first time in three years, with average viewing figures for January 2010 of 10.8 million (40.4% audience share) compared to *Coronation Street*'s 10.4 million (38.2%). Overnight figures for the live episode indicated that it averaged 14.91 million viewers and a 54.6% audience share, peaking at 16.58 million with a 59.4% share in the final five minutes of broadcast when Stacey was revealed as the killer. The 10:30 pm repeat of the episode on BBC Three drew a further 1.42 million viewers, attaining a 7.7% share. *EastEnders Live: The Aftermath* drew 4.3 million viewers and a 15.9% audience share, becoming BBC Three's highest rated programme ever, as well as the most-watched multichannel programme of the day. The documentary attained a further 1.21 million viewers and a 9.4% share upon its repeat at 11 pm. Santer was delighted by the viewing figures, stating: "To get this incredible response from the audience is truly remarkable – these numbers go far beyond what we ever hoped for. I am so proud of our cast and crew for their incredible performance last night. This rating is the icing on our silver anniversary cake." Jay Hunt, controller of BBC One commented: "\[The\] extraordinary live episode was a fitting celebration of 25 magnificent years for *EastEnders*. The audience were clearly gripped by one of the greatest soap whodunnits ever." Discussing the ratings for *EastEnders Live: The Aftermath*, controller of BBC Three Danny Cohen appraised: "It is an amazing testament to the *EastEnders* team and the brave and brilliant drama they provided."

Archie's murder was compared to that of Den Watts in *EastEnders* in 2005 by Polly Hudson of the *Daily Mirror*, while Nancy Banks-Smith of *The Guardian* called it a rip-off of *Citizen Kane*. Andrew Grimes from *Manchester Evening News* said the Christmas Day episode was "in every sense compelling, and to my utter astonishment, a complete and utter joy", and John Gibson of *Edinburgh Evening News* gave the murder discovery episode on 26 December 2009 a negative review, saying "Hard to tell what was most horrific ... the murder, which was bloody, the acting, which was dire, or the script, which was torture." Tim Teeman of *The Times* called the revelation of Stacey as Archie's killer a "genuine surprise", while Pat Stacey of *The Evening Herald* felt that revealing Stacey as Archie's killer was "a slight let-down" and "a little bit predictable". The storyline was nominated in the Killer Secret category at the 2010 All About Soap Bubble Awards. It also received a nomination in the Best Storyline category at the 2010 British Soap Awards and the Best Soap Storyline category at the 2010 TVChoice Awards. Real life police detectives criticised the portrayal of detectives in the show, saying that viewers who see them talking to residents about the case and accepting bribes may believe they operate that way in reality. The BBC insisted that a police consultant was used, adding that "this is heightened fiction and all the things that we show might not always represent real life." The storyline was referenced by Prime Minister Gordon Brown when referring to allegations of bullying, saying "The only thing I haven't been accused of is murdering that guy Archie Mitchell in *EastEnders*."

Bookmakers estimated that over £1 million would be spent gambling on the outcome of the storyline. Ladbrokes experienced its busiest ever 24 hours of gambling on a television series ahead of the episode's transmission, taking £100,000 in bets on 30 different characters, while William Hill took £500,000, surpassing the amount placed on *Dallas*'s Who shot J.R.? storyline in 1980. Spokesman Rupert Adams commented: "The BBC were amazing keeping this quiet. We have broken even which in a market like this is amazing. We have had a roller-coaster but have enjoyed every minute."


title: Wilfrid Woods

abstract: Admiral Sir Wilfrid John Wentworth Woods, was a Royal Navy officer who served in the Submarine Service in the Mediterranean.

text:
# Wilfrid Woods

Admiral **Sir Wilfrid John Wentworth Woods**, GBE, KCB, DSO & Bar, DL (9 February 1906 – 1 January 1975) was a Royal Navy officer who served in the Submarine Service in the Mediterranean.

## Early life

Wilfrid Woods was born on 19 February 1906 at Southsea in Hampshire to colonial administrator Sir Wilfrid Woods KCMG, KBE and Ethel Maud Palmer. He attended school at Seabrooke Lodge at Hythe before going to the Royal Naval College, Osborne and the Britannia Royal Naval College.

## Royal Navy

### Pre-war service

Woods was commissioned into the Royal Navy as a sub-lieutenant in 1926 and specialised in submarines. His first submarine command came in 1935 as a lieutenant in HMS *Seahorse* before promotion to lieutenant-commander in HMS *Nelson* a year later. He then attended the Royal Navy Staff College in 1939.

### Second World War

With the outbreak of the Second World War, Woods was serving on the staff of the Sixth Submarine Flotilla in UK waters before moving to the Mediterranean theatre in HMS *Triumph* in 1940. For his work in Triumph he was awarded the DSO and bar as well as the White Eagle of Yugoslavia. Woods moved to become staff officer (operations) on the staff of the Commander in Chief, Mediterranean.

Leaving the Mediterranean to participate in Operation Overlord he was appointed to command HMS *Centurion*. The ship was scuttled as part of a Mulberry Harbour.

### Post war service

HMS *Forth* was his next command along with command with the 3rd Submarine Flotilla. His career took him on to Chief Staff Officer to Flag Officer Submarines in 1947. He went to the Imperial Defence College in 1951 following a period as Director of Torpedo, Anti-submarine and Mine Warfare. A return to the sea came with the command of HMS *Indomitable* and then back to the Mediterranean as chief of staff to the commander in chief. He was promoted from commodore to rear-admiral in 1955.

Woods' next appointment saw him serve as Flag Officer Submarines from December 1955 to November 1957. From there he was promoted to vice-admiral in 1958 and made NATO Deputy Supreme Allied Commander, Atlantic. He rose to the rank of admiral in July 1960 and appointed to the post of Commander in Chief Home Fleet and then NATO Commander in Chief, Eastern Atlantic Area. In May 1962 he was made First and Principal Naval ADC to Queen Elizabeth II.

He was Commander in Chief, Portsmouth and Allied Commander in Chief, Channel between 1963 and his retirement in 1965.

## Later life

After retiring from the Royal Navy, he was Deputy Lieutenant for Hampshire and spent four years as chairman of the RNLI. During his chairmanship the boat building programme was expanded and a £400,000 deficit cleared.

## Bibliography

## InfoBox

| Admiral
Sir Wilfrid Woods
GBE, KCB, DSO & Bar, DL | |
| --- | --- |
| Born | (1906-02-19)19 February 1906
Southsea, Portsmouth |
| Died | 1 January 1975(1975-01-01) (aged 68)
Burley, Hampshire |
| Allegiance | United Kingdom |
| Service/branch | Royal Navy |
| Years of service | 1926–1965 |
| Rank | Admiral |
| Commands | Commander-in-Chief, Portsmouth (1963–65)
Home Fleet (1960–63)
Flag Officer Submarines (1955–57)
HMS *Indomitable* (1952–53)
3rd Submarine Flotilla (1945–46)
HMS *Forth* (1945–46)
HMS *Centurion* (1944)
HMS *Triumph* (1940–41)
HMS *Seahorse* (1935–36) |
| Battles/wars | Second World War |
| Awards | Knight Grand Cross of the Order of the British Empire
Knight Commander of the Order of the Bath
Distinguished Service Order & Bar
Order of the White Eagle (Yugoslavia)
Grand Commander of the Royal Order of George I (Greece) |
| Alma mater | Royal Naval College, Osborne, Britannia Royal Naval College |
| Relations | Wilfrid Wentworth Woods (Father) |
| Other work | Commodore RN Sailing Association (1963–66)
Chairman, RNLI (1968–72)
President, Sea Cadet Corps Sports Council (1966)
Chairman, Foudroyant Trust (1967)
Deputy Lieutenant of Hampshire |


title: Proview International Holdings

abstract: Proview International Holdings Ltd was a Hong Kong–based manufacturer of computer monitors and other media devices. The company marketed its products under its own and other brand name through its extensive distribution network over the world. Proview manufactured CRT and LCD monitors, LCD TVs, Plasma TVs and DVD players. Proview had production facilities located in Shenzhen and Wuhan in China, as well as in Brazil and Taiwan. Proview held the "iPad" trademark for China and sued Apple for US$1.6 billion in damages. Apple countered that the suit was a shakedown to prop up the company due to its significant debt and impending collapse. Apple ended the dispute with a $60 million payment to Proview. Proview has been delisted from the stock market and the surviving group have not been able to return to business as of May 2023. Their website is no longer online.

text:
# Proview International Holdings

**Proview International Holdings Ltd** (SEHK: 334; Chinese: 唯冠) was a Hong Kong–based manufacturer of computer monitors and other media devices. The company marketed its products under its own and other brand name through its extensive distribution network over the world. Proview manufactured CRT and LCD monitors, LCD TVs, Plasma TVs and DVD players. Proview had production facilities located in Shenzhen and Wuhan in China, as well as in Brazil and Taiwan.

Proview held the "iPad" trademark for China and sued Apple for US$1.6 billion in damages. Apple countered that the suit was a shakedown to prop up the company due to its significant debt and impending collapse. Apple ended the dispute with a $60 million payment to Proview.

Proview has been delisted from the stock market and the surviving group have not been able to return to business as of May 2023. Their website is no longer online.


title: Wilfrid Worland

abstract: Wilfrid V. Worland (1907–1999) was an architect who between the 1930s and the 1990s shaped the suburban landscape of Washington, D.C., by specializing in town houses and who designed two developments named for him --"Worland", a five-story apartment building on Wisconsin Avenue in Washington, D.C., and a town house cluster also called "Worland" on Democracy Boulevard in Bethesda, Md. The 41-unit Wisconsin Avenue project is the only Washington apartment house named for its architect, considered one of Washington's most distinguished addresses.

text:
# Wilfrid Worland

**Wilfrid V. Worland** (1907–1999) was an architect who between the 1930s and the 1990s shaped the suburban landscape of Washington, D.C., by specializing in town houses and who designed two developments named for him --"Worland", a five-story apartment building on Wisconsin Avenue in Washington, D.C., and a town house cluster also called "Worland" on Democracy Boulevard in Bethesda, Md. The 41-unit Wisconsin Avenue project is the only Washington apartment house named for its architect, considered one of Washington's most distinguished addresses.

## Career

Among the thousands of brick colonial and federal-style homes he designed since the 1930s were parts of Woodacres and the entire neighborhoods of Fallsreach, Falls Mead, Luxmanor, Old Farm and Westbard Mews in Maryland. He also designed the neighborhoods of Lake Ridge, Falcon Ridge, Carlyle Walk and Afton Glen, all in Virginia.

Among the nonresidential structures Worland helped design was Our Lady of Lourdes Catholic Church in Bethesda, Md.

In the late 1940s, Worland formed a partnership with architect Michael A. Patterson. The firm, Patterson & Worland, created the designs for many of the homes in Montgomery Village (1967), a planned community designed by the Kettler Brothers. Patterson & Worland, became Worland Associates after Patterson retired in 1978. Worland retired in 1992, and the Rockville-based concern became Hutchinson + Associates.

Explaining the appeal of the colonial style in 1980, Worland told *The Washington Post*, "Many people move here from someplace else. They feel that they need something with a background. The brick colonial is sort of a blanket–it provides security, a feeling of having been established in a community. And it holds its value."

Bob Mitchell, president of the National Association of Home Builders, led a firm that built many of the projects Worland designed. Mitchell said: "Everything he did, particularly his exteriors, were just perfectly in balance." Peerless Rockville Historic Preservation Ltd. gave a Preservation Award in 1985 to Mitchell & Best Co. for a group of five wood-and-brick, condominium-style buildings Worland designed. The structures are called Rockmanor Office Park, at 1686 E. Gude Dr., Rockville, Md., and feature rear balconies overlooking Redgate Municipal Golf Course.

Worland was born in Jasper, Indiana, and was a 1931 architecture graduate of what was then the Carnegie Institute of Technology in Pittsburgh, Pennsylvania. After graduation, he came to the Washington area and began work as an architect.

During World War II, he served in the Corps of Engineers, receiving a Bronze Star and the Legion of Merit. He retired from the Army Reserve as a colonel in 1967.

Worland was a member of the American Institute of Architects and Holy Cross Catholic Church in Garrett Park, Md. His hobbies included gardening and family history.

Worland died December 11, 1999, at his home in Bethesda, Md., of a heart attack. Survivors included his wife of 65 years, Mary Rose Pauly Worland in Bethesda (originally from Falls Church, Virginia); two daughters, Kathleen Hamm, in Bethesda, and Paula Lipsitz, in Tucson; two sons, Julien, in St. Louis, and Wilfrid, in British Columbia; his youngest brother, Donovan, in San Francisco; and 11 grandchildren.

Worland was a co-author (with Olive Lewis Kolb and Vincent Worland) of *One Man's Family: The Genealogy of the Worland Family in America, 1662–1962* published privately in 1968 and available as a PDF. He was the posthumous author of *Jasper Remembered: An Oral History of the Early 1900s in Southern Indiana,* published in 2010, which is available from the Dubois Co. Historical Museum, Jasper, Ind.

## Sources

* Bernstein, Adam. "Architect Wilfrid Worland Dies at 92." *The Washington Post*, Tuesday, December 14, 1999, Page B07.
* Goode, James M. *Best Addresses: A Century of Washington's Distinguished Apartment Houses.* Smithsonian Institution Press, Washington, D.C., 1988.


title: Prozor-Rama

abstract: Prozor-Rama is a municipality located in Herzegovina-Neretva Canton of the Federation of Bosnia and Herzegovina, an entity of Bosnia and Herzegovina. Its seat is Prozor. Also, Ramsko lake is located in the municipality.

text:
# Prozor-Rama

**Prozor-Rama** (Serbian Cyrillic: Прозор-Рама) is a municipality located in Herzegovina-Neretva Canton of the Federation of Bosnia and Herzegovina, an entity of Bosnia and Herzegovina. Its seat is Prozor. Also, Ramsko lake is located in the municipality.

## History

In the Middle Ages, the King of Hungary held the title of King of Rama named after this region.

## Demographics

North Herzegovina

According to the 2013 census, the population of the municipality was 14,280 and of the seat Prozor 3,367.

### 2013

14,280 total

### Settlements

Towns and settlements in the municipality are Blace, Borovnica, Dobroša Donja Vast, Donji Krančići, Donji Višnjani, Družinovići, Duge, Gmići, Gorica, Gornji Krančići, Gornji Višnjani, Gračac, Gračanica, Grevići, Heljdovi, Here, Hudutsko, Ivanci, Jaklići, Klek, Kovačevo Polje, Kozo, Kućani, Kute, Lapsunj, Lizoperci, Ljubunci, Lug, Maglice, Meopotočje, Mluša, Ometala, Orašac, Pajići, Parcani, Paroš, Ploča, Podbor, Proslap, Prozor, Ravnica, Ripci, Rumboci, Šćipe, Šćit, Šerovina, Skrobućani, Šlimac, Tošćanica, Trišćani, Ustirama, Uzdol, Varvara and Zahum.

## Sports

The area is home to the football club HNK Rama, and basketball club HKK Rama.

## Notable people

## InfoBox

| Prozor-Rama Прозор-Рама | |
| --- | --- |
| Town and municipality | |
| Panoramic view | |
|  | |
| Location of Prozor-Rama within Bosnia and Herzegovina. | |
| Prozor-Rama | |
| Coordinates: 43°49′12″N 17°36′36″E / 43.82000°N 17.61000°E / 43.82000; 17.61000 | |
| Country | Bosnia and Herzegovina |
| Entity | Federation of Bosnia and Herzegovina |
| Canton | Herzegovina-Neretva |
| Geographical region | Herzegovina |
| Government | |
| Municipal mayor | Jozo Ivančević (Ind.) |
| Area | |
| Town and municipality | 477 km2 (184 sq mi) |
| Population (2013 census) | |
| Town and municipality | 14,280 |
| Density | 34/km2 (90/sq mi) |
| Urban | 3,367 |
| Time zone | UTC+1 (CET) |
| Summer (DST) | UTC+2 (CEST) |
| Area code | +387 36 |
| Website | www.prozor-rama.org |


title: Proctoporus carabaya

abstract: Proctoporus carabaya is a species of lizard in the family Gymnophthalmidae. It is endemic to Peru.

text:
# Proctoporus carabaya

***Proctoporus carabaya*** is a species of lizard in the family Gymnophthalmidae. It is endemic to Peru.

## InfoBox

| *Proctoporus carabaya* | |
| --- | --- |
|
| Scientific classification | |
| Domain: | Eukaryota |
| Kingdom: | Animalia |
| Phylum: | Chordata |
| Class: | Reptilia |
| Order: | Squamata |
| Family: | Gymnophthalmidae |
| Genus: | *Proctoporus* |
| Species: | ***P. carabaya*** |
| Binomial name | |
| ***Proctoporus carabaya***<br>Goicoechea, Padial, Chaparro, Castroviejo-Fisher, & De la Riva, 2013 | |
|


title: Willardiine

abstract: Willardiine (correctly spelled with two successive i's) or (S)-1-(2-amino-2-carboxyethyl)pyrimidine-2,4-dione is a chemical compound that occurs naturally in the seeds of Mariosousa willardiana and Acacia sensu lato. The seedlings of these plants contain enzymes capable of complex chemical substitutions that result in the formation of free amino acids (See: #Synthesis). Willardiine is frequently studied for its function in higher level plants. Additionally, many derivates of willardiine are researched for their potential in pharmaceutical development. Willardiine was first discovered in 1959 by R. Gmelin, when he isolated several free, non-protein amino acids from Acacia willardiana (another name for Mariosousa willardiana) when he was studying how these families of plants synthesize uracilyalanines. A related compound, Isowillardiine, was concurrently isolated by a different group, and it was discovered that the two compounds had different structural and functional properties. Subsequent research on willardiine has focused on the functional significance of different substitutions at the nitrogen group and the development of analogs of willardiine with different pharmacokinetic properties. In general, Willardiine is the one of the first compounds studied in which slight changes to molecular structure result in compounds with significantly different pharmacokinetic properties. Willardiine is a partial agonist of Ionotropic glutamate receptors. These receptors are found at excitatory synapses and bind glutamate (the major excitatory neurotransmitter) and structurally similar ligands, such as willardiine. Receptor activation leads to influx of positive ions into the neuron, resulting in neural depolarization (See: #Structure and Activity). Willardiine specifically agonizes non-NMDA glutamate receptors: AMPA and kainate receptors. Willardiine analogs have been developed that have different binding affinities for the AMPA and kainate receptors. These analogs have been used to study the structure of these receptors, as well as the functional significance of receptor activation in different brain regions. While willardiine and its analogs have not been explicitly studied as therapeutics, there are a variety of neurological disorders characterized by alterations in glutamate signaling, and ligands for AMPA and kainate receptors are often studied as potential therapeutics.

text:
# Willardiine

**Willardiine** (correctly spelled with two successive i's) or **(*S*)-1-(2-amino-2-carboxyethyl)pyrimidine-2,4-dione** is a chemical compound that occurs naturally in the seeds of *Mariosousa willardiana* and *Acacia* sensu lato. The seedlings of these plants contain enzymes capable of complex chemical substitutions that result in the formation of free amino acids (*See:* #Synthesis). Willardiine is frequently studied for its function in higher level plants. Additionally, many derivates of willardiine are researched for their potential in pharmaceutical development. Willardiine was first discovered in 1959 by R. Gmelin, when he isolated several free, non-protein amino acids from *Acacia willardiana* (another name for *Mariosousa willardiana*) when he was studying how these families of plants synthesize uracilyalanines. A related compound, Isowillardiine, was concurrently isolated by a different group, and it was discovered that the two compounds had different structural and functional properties. Subsequent research on willardiine has focused on the functional significance of different substitutions at the nitrogen group and the development of analogs of willardiine with different pharmacokinetic properties. In general, Willardiine is the one of the first compounds studied in which slight changes to molecular structure result in compounds with significantly different pharmacokinetic properties.

Willardiine is a partial agonist of Ionotropic glutamate receptors. These receptors are found at excitatory synapses and bind glutamate (the major excitatory neurotransmitter) and structurally similar ligands, such as willardiine. Receptor activation leads to influx of positive ions into the neuron, resulting in neural depolarization (*See:* #Structure and Activity). Willardiine specifically agonizes non-NMDA glutamate receptors: AMPA and kainate receptors.

Willardiine analogs have been developed that have different binding affinities for the AMPA and kainate receptors. These analogs have been used to study the structure of these receptors, as well as the functional significance of receptor activation in different brain regions. While willardiine and its analogs have not been explicitly studied as therapeutics, there are a variety of neurological disorders characterized by alterations in glutamate signaling, and ligands for AMPA and kainate receptors are often studied as potential therapeutics.

## Chemistry

### Structure and activity

#### Structure

Willardiine was isolated from *Acacia Willardiana* and characterized as 3-(1-uracyl)-L-alanine, based on elemental composition and stability in strong acid, which were used to deduce the organic structure of willardiine (*Figure 1)*.

The experimentally derived properties of willardiine are similar to L-albizziine, which was isolated from the same seed. Subsequent synthetic work proved the structure and properties of willardiine (*see:* #Synthesis).

The family of willardiine compounds (*see:* #Analogs) all have a uracil or substituted uracil as the primary amino acid side chain. Willardiine naturally exists as two isomers:

* (*S*)-Willardiine
* (*R*)-Willardiine

Only the (*S*) isomer has binding affinity for the AMPA and kainate receptors. Isomer-specific binding affinity is a result of steric effects between (*R*)-Willardiine and the binding site on the receptor.

#### Activity

AMPA receptors are tetrameric transmembrane proteins with distinct amino terminal, ligand binding, and transmembrane domains (*Figure 2)*. They are expressed on postsynaptic membranes on neurons, and are expressed widely throughout the brain. Willardiine binds to glutamate receptors at the glutamate binding site in the extracellular ligand binding domain (*Figure 2).* Binding causes a conformational change that opens the receptor and allows for positively charged ions, Na+ and/or Ca2+ to enter the cell\** (*Figure 3)*. This depolarizes, and activates, the neuron, resulting in the firing of an action potential. The ion can also initiate a signaling cascade to activate different types of proteins that influence the cell, such as kinases or transcription factors.

\**Passage of calcium through the AMPA receptor ("calcium permeability") is based on the presence of the edited GluA2 subunit (*See: Glur2 RNA editing*). The ion pore region of GluA2 mRNA is edited during translation to render it calcium impermeable in over 99% of AMPA receptors.

Like AMPA receptors, kainate receptors are tetrameric, transmembrane, ionotropic glutamate receptors on glutamatergic neurons. They have five subunits, divided into two main families: GluK1,2, and GluK5,6,7. An endogenous ligand, either kainic acid or glutamate, binds to the ligand binding site. However, unlike AMPA receptors, external ions also bind to kainate receptors at the ion binding pocket on the extracellular domain. When both the ligand and ion bind, the receptor undergoes a conformational change and the ion channel opens. This allows the flow of positive ions, such as sodium or calcium. The influx of positively charged ions depolarizes, or excites, the neuron (*Figure 4)*. Like AMPA receptors, the permeability to calcium is dependent on the editing of receptor subunit mRNA. The rise and decay times of postsynaptic potentials is much slower in kainate receptors than AMPA receptors.

Kainate receptors are much less ubiquitously expressed throughout the brain and have a less significant role in plasticity than AMP receptors. In general, the function of kainate receptors is much less characterized than AMPA receptors. Interestingly, kainate receptors are expressed on the presynaptic membrane as well as the postsynaptic membrane. It is believed that presynaptic expression mediates the amount of neurotransmitter released from the cell (*Figure 4).* It is also known that kainic acid can induce seizures.

Both kainate and AMPA receptors are also affected by a variety of exogenous ligands, including willardiine. Only the (S) isomer of willardiine is a potent agonist of non-NMDA glutamate receptors. The precise binding has been characterized on cloned AMPA and Kainate receptors by analyzing the amount of displaced radiolabelled agonist (AMPA and kainate, respectively), which represents the binding affinity of willardiine to the receptor. (S)-willardiine displaces significantly less AMPA/kainate than its analogs, such as 5-Fluorowillardiine or 5-Iodowillardiine. Willardiine has the strongest binding affinity at AMPA subunit GluR4 and the kainate receptor subunit GluK5.

The displacement of glutamate by willardiine is primarily exothermic, with favorable binding enthalpy of -5±1 kCal/mol.

The structure and activity of willardiine were determined through elucidating the natural synthesis of willardiine and creating a synthetic mechanism of synthesis that can be used to create willardiine and its analogs to be studying *in vitro* and *in vivo*.

### Synthesis

The natural synthesis of willardiine and Isowillardiine from seedlings has been characterized (*Figure 5)*. The synthesis consists of a free uracil ring at nitrogen being substituted for an alanyl side chain, derived from *O*-acetyl-*L*-serine.

The synthesis of willardiine has also been replicated *in vitro,* in which willardiine is synthesized from linear urea, which is made from a solution of acyl isocynate in Benzene with aminoacetaldehyde. Linear urea is cyclized to uracil when treated with aqueous alkali. Hydrolysis of uracil with Hydrochloric acid gives uracil-1-ylacetaldehyde. Hydrolysis of uracil-1-ylacetaldehyde with Potassium cyanide, Ammonia, and Ammonium chloride give the final structure of willardiine. This final synthesis of willardiine from uracil-1-lyacetaldehyde is carried out under the conditions of Strecker amino acid synthesis (*Figure 5)*.

The lower binding affinity of willardiine for the AMPA and kainate receptors can be attributed to the unsubstituted carbon on position 5 of the 6-membered ring. Substitutions of large, electron-withdrawing groups at this position increase the affinity for kainate receptors but decrease the binding affinity for AMPA receptors. An example of the synthesis of one analog, 5-bromowillardiine, is shown in *Figure 6*.

Derivatives of willardiine have also been developed as Kainate receptor antagonists. These were synthesized through the addition of substituents to the N3 position of the 6-membered ring on the natural product willardiine (*Figure 7)*.

### Analogs

#### Agonists

The most common analogs of willardiine are also agonists of AMPA and kainate receptors. Each analogs differs in the substitution at the 5th position on the six-membered ring, and the most commonly studied analogs have a halogen at this position which is added through a Halogen addition reaction (*Figure 6)*. The addition of a halogen affect the binding affinities and stability of the analogs. The analogs are more stable than unsubstituted willardiine and have better binding affinity for AMPA receptors, though the chemistry underlying the change in binding mechanisms remains unknown.

#### Antagonists

Derivative of willardiine have been developed as synthetic kainate and AMPA receptor antagonists (*See:* #Synthesis for specifics on development of antagonists).

* UBP282 (*R = 4-COOH, (S))*
* UBP296 (*R = 2-COOH, (R/S))*
* UBP302 (*R = 4-COOH, (S))*

These glutamate receptor antagonists all share a carboxylbenzyl substitution on the six-membered ring (*Figure 7)*. UBP296 and UBP302 have been shown to have a 100-fold increase in binding kainate receptors over AMPA receptors, but UBP282 has competitive affinity for GluA2-containing AMPA receptors and GluK1-containing kainate receptors. These antagonists have therapeutic potential for a variety of neurological disorders characterized by aberrant activation of AMPA or kainate receptors (*See:* #Disease relevance). The pharmacokinetics of the compounds must be elucidated before they can be studied as potential therapeutics.

### Pharmacokinetics

It is crucial to understand the pharmacokinetics of any compound that has the potential to be developed as a therapeutic. These properties describe the ADME properties of the compound, which will determine the route of administration, dose, and potential adverse effects of a drug. The pharmacokinetic properties of willardiine have been studied using whole-cell recordings of mouse embryonic neurons. Willardiine desensitizes AMPA receptors with an EC50 of 44.8 uM, which makes it 4 times less potent that AMPA (EC50 = 11 uM), and 30 times less potent than its analog 5-Fluorowillardiine (EC50 = 1.5 uM).

Many of the pharmacokinetic properties of willardiine remain unknown due to a lack of *in vivo* or clinical research. Specific ADME properties have been predicted using admetSAR, a free tool that predicts properties of absorbance, distribution, metabolism, and excretion (*Table 1)*.

The pKa of willardiine is approximately 10, meaning that willardiine is uncharged, or protonated, at physiological pH.

Table 1. Predicted pharmacokinetic properties of willardiine
| PROPERTY | VALUE | SOURCE |
| --- | --- | --- |
| Water solubility | 13.2 mg/mL | ALOGPS |
| logP | -0.7 | ALOGPS |
| logP | -1.3 | ChemAxon |
| logS | -1.2 | ALOGPS |
| pKa (Strongest Acidic) | 9.76 | ChemAxon |
| pKa (Strongest Basic) | 2.97 | ChemAxon |
| Physiological Charge | 0 | ChemAxon |
| Hydrogen Acceptor Count | 4 | ChemAxon |
| Hydrogen Donor Count | 2 | ChemAxon |
| Polar Surface Area | 101.73 Å2 | ChemAxon |
| Rotatable Bond Count | 4 | ChemAxon |
| Refractivity | 46.01 m3·mol-1 | ChemAxon |
| Polarizability | 17.89 Å3 | ChemAxon |
| Number of Rings | 1 | ChemAxon |
| Bioavailability | 1 | ChemAxon |
| Rule of Five | Yes | ChemAxon |
| Ghose Filter | No | ChemAxon |
| Veber's Rule | No | ChemAxon |
| MDDR-like Rule | No | ChemAxon |

## Applications in research

Willardiine and its analogs bind to AMPA and Kainate receptors. These glutamate receptors are the primary mediators of excitation in the central nervous system, and are commonly studied in hippocampal or cortical neurons. Because of their different binding affinities for each receptor, members of the willardiine family have been used to determine the structural/function consequences of activation of AMPA/kainate receptors by different agonists or antagonists. Additionally, in rat spinal motor neurons, it was demonstrated that different analogs of willardiine affected different non-NMDA glutamate receptors. This finding contributed to the discovery of kainate and AMPA receptors as two structurally and functionally different receptors.

### Structure assays

Crystallography studies of AMPA receptors in the willardiine-bound state have shown how the conformation of the receptor changes throughout the binding, resulting channel activation, and unbinding of a partial agonist. These studies found that the efficacy of the agonist was directly correlated to the extent of domain closure. These crystallography studies were performed with a variety of 5-position halogen-substituted willardiine analogs to show that steric hindrance influences the extent of domain closure.

Willardiine and its analogs have been used to study the effects of partial agonism on the structure and function of AMPA receptors. Single channel recording of willardiine binding to AMPA receptors showed the fraction of time that the ion channel spends in an open state. These experiments gave important insight into the structure of AMPA receptors when a partial agonist is bound, as compared to a full agonist or antagonist.

Additionally, derivatives of willardiine with an additional carboxyl group (*Figure 6)* are potent AMPA and/or kainate receptor antagonists. Slight differences in the position of the substitution significantly changes the binding affinity for the receptors. The synthetic antagonists also have different affinities for each subunit of the kainate and AMPA receptors. Thus, the synthetic UBP antagonists can be used to study the structural elements of each binding site that are important for activation or inhibition of the receptor based on the subunit.

### Functional assays

Willardiine and its analogs can be used to study the effects of AMPA and kainate receptor activation or inhibition on neuronal activity and animal behavior. AMPA receptors activate neurons due to the influx of sodium and sometimes calcium after the binding of a ligand to the ligand binding domain (*figure 3)**.* Kainate receptors also transmit positive ions, but the resulting change in postsynaptic potential is less pronounced than that of an AMPA receptor. As a partial agonist, willardiine could be applied electrophysiology studies of neurons to determine the specific changes in neuronal activity (as represented by electrical signals) when a partial agonist is bound.

Another way to track the activity of the receptors is through calcium imaging. Both kainate and AMPA receptors have different permeability for calcium based on the four subunits of the tetramer. For example, AMPA receptors are only permeable to calcium if the receptor is GluA2-lacking or contains unedited GluA2. Calcium imaging in the presence of willardiine and related analogs could differentiate what receptor subtypes are activated by each agonist or inhibited by each antagonist. This could further the understanding of the specific role of calcium permeable non-NMDA glutamate receptors.

The synthetic antagonists can be used to better understand the neuronal functions of kainate receptors. The functions of kainate receptors are not well characterized because of the lack of specific antagonists for the receptors. Two of the UBP antagonists have been determined to have high, specific binding affinity for kainate receptors. These antagonists can be used to study the contribution of kainate receptors on neuronal activity and behavior.

### Localization assays

Radio-labeled willardiine has been used to study the distribution of AMPA and Kainate receptors in the brain, based on its function as both an AMPA receptor and Kainate receptor agonist.

### Behavioral/disease model assays

A combination of functional, structural, and localization assays of willardiine and its analogs can be used to research a variety of neurological diseases that are characterized by dysregulated glutamate signaling, such as Parkinson's disease, Alzheimer's disease, or amyotrophic lateral sclerosis (ALS) (*See:* #Disease relevance).

Many neurological diseases have been studied using mouse models of human disease. These are mouse lines that have the pathological genotype of the respective disease. As a result, the mice can be used to study phenotypes caused by the disease. Mice can be given an injection or oral suspension of willardiine or an analog. Then, behavioral assays will determine if the compound is helpful in alleviating symptoms of the relevant disease. Different doses and formulations of the compound will help identify potential therapeutic applications and any dose-dependent affects. While willardiine has not been explicitly used to study behavior, AMPA receptors are frequently activated in behavioral studies to observe the effects of activation on development, learning, memory, and neurological disease (*See:* **Potential Therapeutic Applications)****.**

The aforementioned research could also help understand the potential application of willardiine and its more potent analogs and derived antagonists in treating neurological disease.

## Disease relevance

Willardiine and its analogs bind specifically to AMPA and kainate receptors, which are implicated in a variety of neurological disorders. The following section describes a few neurological diseases characterized by dysregulation in either AMPA or kainate receptor activation. This list is not exhaustive, and research in these fields is in constant development.

### AMPA receptors in disease

#### Neurodegenerative disorders

AMPA receptors have an extensive physiological role in synaptic plasticity, which is the basis for many aspects of neural development, learning, and memory. Many neurodegenerative disorders are characterized by cognitive decline, which is mediated by changes in AMPA-mediated plasticity. This could be due to changes in AMPA receptor expression, trafficking, or activity in regions like the Hippocampus or Striatum. Combinations of the three processes have been shown to be dysregulated in animal models of Alzheimer's disease, Huntington's disease, and Parkinson's disease.

Animal models of Parkinson's disease have shown elevated levels of AMPA receptors in affected regions. While AMPA antagonism has been study as a potential treatment, the off-target effects of inhibiting AMPA receptors are too severe to justify the benefits towards symptoms of Parkinson's.

AMPA receptor deficits have been studied in animal models and human postmortem tissue of Huntington's disease. Expression of mutant Huntingtin impairs AMPA-mediated synaptic transmission by disrupting subunit transport across microtubules. Modulation of AMPA receptors in animal models of Huntington's disease have reduced degeneration in the striatum and reduced memory deficits.

#### Autism spectrum disorders

AMPA receptors role in synaptic plasticity is important not only for cognitive abilities but also in neural development. Expression of AMPA receptors, as well as NMDA receptors follows a specific sequence during development to differentially develop or silence synaptic connections. Incorrect expression or function of AMPA receptors during development can result in aberrant or incomplete synaptic connections, which can negatively impact cognitive development and result in intellectual disabilities.

There are reports of genetic alterations in humans with Autism spectrum disorders that result in hemizygosity of the GluA2 subunit, which is crucial for mediating calcium permeability of the AMPA receptor. There are also genetic alterations in expression of proteins in the postsynaptic density that are crucial for the anchoring of the receptor to the membrane. Human GRIP1, SHANK3 (as well as other members of the SHANK family), and E3 Ubiquitin Ligase all have identified mutations in Autism Spectrum Disorders that dysregulate AMPA synaptic expression.

The role of AMPA (and possibly kainate) receptors in Autism Spectrum Disorders is also supported by the therapeutic effectiveness of Topiramate, an AMPA/kainate receptor antagonize, in children with autism, pervasive developmental disorder, and obsessive–compulsive disorder. In multiple retrospective cohort studies, it was found that adolescent patients of these diseases had significant, positive changes in social conduct, hyperactivity, and attention with minor side effects.

#### Major depressive disorder

Similar to autism spectrum disorders, major depressive disorder has a variety of symptoms and etiologies that make it difficult to find a common molecular cause. There are many hypotheses about the biological basis of depression, including the glutamate hypothesis. This hypothesis was corroborated by evidence that NMDA antagonists have antidepressant effects in rodents. There are many NMDA antagonists currently being used in clinical studies that have safe, rapid antidepressant effects. A notable example is the novel use of Ketamine as a rapid onset antidepressant. It is hypothesized that ketamine exerts its effects by blocking the activation of NMDA receptors, thus forcing the activation of AMPA receptors to compensate for lost synaptic glutamate. It remains unclear how AMPA activation results in antidepressant outcomes, but studies of AMPA agonists as potential therapeutic targets for depression have had promising preclinical results.

A major symptom of major depressive disorder is dysregulated sleep, which has recently been discovered to be mediated in part by AMPA receptors. AMPA receptors are selectively calcium permeable, based on the presence and amino acid composition of GluA2 (*See*: **Activity**). Trafficking of calcium permeable AMPA receptors (CP-AMPARs) is modulated during the sleep/wake cycle, although the mechanism is still not clear.

### Kainate receptors in disease

#### Mood disorders

The role of kainate receptors in mood disorders is not well elucidated and studies are often contradictory. Postmortem studies have found a decrease in GluK1 mRNA in the prefrontal cortex and hippocampus of patients with Schizophrenia. However, this has not been corroborated by other studies. Alternatively, some studies have found a decrease in GluK2, but not GluK1, mRNA in the prefrontal cortex of schizophrenia patients.

Genome-wide association studies of thousands of cases of schizophrenia have identified a single-nucleotide polymorphism (SNP) in the *grik4* gene that alters gene expression. This SNP is more abundant in patients with bipolar disorder that respond to certain forms of medication (namely, selective serotonin reuptake inhibitors) over other forms of medication. This result suggests a role of differentially expressed GluK4 in bipolar disorder and responses to medication, but research into the specific mechanism is still ongoing. *GriK2* knockout mice have shown increased hyperactivity, indicative of bipolar mania. There is no evidence, however, that GluK2 is part of the pathophysiology or just related to the symptoms.

#### Neuropathic pain

Kainate receptors are expressed throughout the dorsal root ganglion and dorsal horn in the spinal cord, which are crucial intermediary regions for transmission of sensory stimulation and pain. Molecular and electrophysiological characterization of these receptors shows that they are heteromeric receptors made up of GluK1 and GluK5 subunits. The activation of primary afferents results in activation of kainate receptor-mediated excitatory postsynaptic potentials on dorsal horn neurons, suggesting that kainate receptors are mediating the pain response.

#### Epilepsy

Epilepsy is characterized by imbalances in the ratio of neuronal excitation and inhibition. It is well characterized that injection of kainic acid can induce seizures, including temporal lobe epilepsy months after injection. It is thought that the increase of kainate receptor activation causes the formation of aberrant synapses in the hippocampus and other areas that are considered to have a low epileptogenic threshold. These aberrant synapses contain kainate receptors and increase the excitation of the brain region, which can induce excitotoxicity and seizures.

Consistent with these findings, transgenic mice with knocked out GluK1 have reduced seizures after treatment with kainic acid. GluK1 antagonists have been beneficial in preventing seizures in the hippocampus of mice (*See:* **Potential therapeutic applications**). In contrast, some research has produced promising results studying GluK1 agonists as treatment for epilepsy. These agonists are hypothesized to decrease the over-inhibition of hippocampal interneurons that is thought to be characterized of epilepsy.

The variety of linkages between kainate receptors and epilepsy demonstrate the difficulty in studying kainate receptors, based on the many hypothesized functions of the receptors. However, these varied and sometimes contradictory mechanisms of action showcase the numerous potentials of a kainate receptor therapeutic that can specifically target one brain region.

## Potential therapeutic applications

### Willardiine-derived agonists

The disease relevance of non-NMDA glutamate receptors suggests a potential for willardiine as a therapeutic. However, since willardiine has a low binding affinity as a partial agonist, it is not commonly studied as a potential therapeutic for diseases characterized by dysregulated receptor expression or activation. Many of its analogs, for example 5-Fluorowillardiine, have increased binding affinity and specificity for either the AMPA and kainate receptor. These properties are more desirable for drug development: a lower dose will be needed to produce a therapeutic effect, and high specificity leads to less off-target or side effects.

AMPA agonists, and potentially willardiine analogs, are most commonly studied as treatments for Major depressive disorder (*See:* **Disease relevance**). Ketamine has a novel indication as an antidepressant for its function as an NMDA-antagonist. The inhibition of NMDA receptors results in increased activity of AMPA receptors, likely to compensate for the decrease in glutamate signaling. Direct AMPA agonists are currently in development as antidepressants, and preclinical studies suggest that these agonists are safe and efficacious *in vitro* and in animal models.

### Willardiine-derived antagonists

The synthetic willardiine-derived kainate antagonists have shown specificity for the kainate receptor. There is evidence that these antagonists could be used to treat neurological disorders that have characteristic over-activation of kainate receptors. Willardiine-derived kainate antagonists have shown efficacy in treating pain, epilepsy, anxiety, ischemia and axonal degeneration.

For example, an antagonist to the GluK1 subunit of the kainate receptor could help prevent with epileptic seizures (*See:* **Disease Relevance**). Antagonists of GluK1 have prevented the development of epileptic activity in the hippocampus of pilocarpine-induced models of epilepsy. Additionally, kainate receptor antagonists have been shown to have analgesic effects in animal models of pain. One antagonist showed increased latency of escape in a hot plate test and decreased the amount of paw licking after exposure to a painful stimuli.

However, many of the willardiine-derived kainate antagonists also antagonize AMPA receptors. Inhibiting AMPA receptors can have severe toxic effects, such as dyskenesia and changes in mood caused by alterations in dopaminergic pathways. Thus, neither willardiine nor its analogs can be pursued as a therapeutic for any aforementioned neurological disorder until the toxicity and adverse effects of the compound are well characterized.

## Toxicity

The research applications and potentials for therapeutics are numerous because of the varied role of non-NMDA glutamate receptors in disease. However, because of their ubiquity in the brain and spinal cord, activation of these receptors can also result in toxic side effects. For this reason, the extracellular levels of AMPA agonists (such as endogenous glutamate) are strictly controlled in the brain and spinal cord. The main side effects of over-activation of AMPA receptors are seizure and neuron death.

There is limited *in vivo* research on the neurotoxicity of willardiine. Due to the low EC50, Willardiine does not induce neurotoxicity at a therapeutic level. Analogs with higher binding affinity, such as 5-Flurowillardiine, have been shown to induce seizure and cell death when administered at high doses.

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## InfoBox

Willardiine
|  | |
| --- | --- |
|
Flowers of *Mariosousa willardiana* | |
| Names | |
| IUPAC name 3-(2,4-Dioxo-3,4-dihydropyrimidin-1(2*H*)-yl)-L-alanine | |
| Systematic IUPAC name (2*S*)-2-Amino-3-(2,4-dioxo-3,4-dihydropyrimidin-1(2*H*)-yl)propanoic acid | |
| Other names * 3-(Uracil-1-yl)-L-alanine * 3-(1-Uracyl)-L-alanine | |
| Identifiers | |
| CAS Number |  |
| 3D model (JSmol) |  |
| Beilstein Reference | 20710 |
| ChEBI |  |
| ChEMBL |  |
| ChemSpider |  |
| DrugBank |  |
| KEGG |  |
| MeSH | Willardiine |
| PubChem CID |  |
| CompTox Dashboard (EPA) |  |
| InChI * InChI=1S/C7H9N3O4/c8-4(6(12)13)3-10-2-1-5(11)9-7(10)14/h1-2,4H,3,8H2,(H,12,13)(H,9,11,14)/t4-/m0/s1Key: FACUYWPMDKTVFU-BYPYZUCNSA-N | |
| SMILES * C1=CN(C(=O)NC1=O)C\[C@@H\](C(=O)O)N | |
| Properties | |
| Chemical formula | C7H9N3O4 |
| Molar mass | 199.166 g·mol−1 |
| log *P* | −4.4 |
| Acidity (p*K*a) | 2.97 |
| Basicity (p*K*b) | 9.76 |
| Except where otherwise noted, data are given for materials in their standard state (at 25 °C \[77 °F\], 100 kPa).  Infobox references | |


title: Protowenella

abstract: Protowenella is a genus of helcionellid from the Middle Cambrian of Australia. It has a strongly spiralled, smooth shell with concentric ridges that have low relief. Other than its tighter coiling, it is very similar to Tichkaella.

text:
# Protowenella

***Protowenella*** is a genus of helcionellid from the Middle Cambrian of Australia. It has a strongly spiralled, smooth shell with concentric ridges that have low relief. Other than its tighter coiling, it is very similar to *Tichkaella*.

## InfoBox

| *Protowenella*<br>Temporal range: | |
| --- | --- |
|
| Scientific classification | |
| Domain: | Eukaryota |
| Kingdom: | Animalia |
| Phylum: | Mollusca |
| Class: | Helcionelloida |
| Order: | Helcionelliformes |
| Superfamily: | Helcionelloidea |
| Genus: | *Protowenella* |
|